Need help? Call us at (833) 966-4233

essay on attention deficit disorder

ADHD is my superpower: A personal essay

Two kids with adult in front of mountain

A Story About a Kid

In 1989, I was 7 years old and just starting first grade. Early in the school year, my teacher arranged a meeting with my parents and stated that she thought that I might be “slow” because I wasn’t performing in class to the same level as the other kids. She even volunteered to my parents that perhaps a “special” class would be better for me at a different school.

Thankfully, my parents rejected the idea that I was “slow” out of hand, as they knew me at home as a bright, talkative, friendly, and curious kid — taking apart our VHS machines and putting them back together, filming and writing short films that I’d shoot with neighborhood kids, messing around with our new Apple IIgs computer!

The school, however, wanted me to see a psychiatrist and have IQ tests done to figure out what was going on. To this day, I remember going to the office and meeting with the team — and I even remember having a blast doing the IQ tests. I remember I solved the block test so fast that the clinician was caught off guard and I had to tell them that I was done — but I also remember them trying to have me repeat numbers back backwards and I could barely do it!

Being Labeled

The prognosis was that I was high intelligence and had attention-deficit disorder (ADD). They removed the hyperactive part because I wasn’t having the type of behavioral problems like running around the classroom (I’ll cover later why I now proudly identify as hyperactive). A week later, my pediatrician started me on Ritalin and I was told several things that really honestly messed me up.

I was told that I had a “learning disability” — which, to 7-year-old me, didn’t make any sense since I LOVED learning! I was told that I would take my tests in a special room so that I’d have fewer distractions. So, the other kids would watch me walk out of the classroom and ask why I left the room when tests were happening — and they, too, were informed that I had a learning disability.

As you can imagine, kids aren’t really lining up to be friends with the “disabled” kid, nor did they hold back on playground taunts around the issue.

These were very early days, long before attention deficit hyperactivity disorder (ADHD) was well known, and long before people had really figured out how to talk to kids with neurodiversities . And as a society, we didn’t really have a concept that someone who has a non-typical brain can be highly functional — it was a time when we didn’t know that the world’s richest man was on the autism spectrum !

Growing Past a Label

I chugged my way through elementary school, then high school, then college — getting consistent B’s and C’s. What strikes me, looking back nearly 30 years later, is just how markedly inconsistent my performance was! In highly interactive environments, or, ironically, the classes that were the most demanding, I did very well! In the classes that moved the slowest or required the most amount of repetition, I floundered.

Like, I got a good grade in the AP Biology course with a TON of memorization, but it was so demanding and the topics were so varied and fast-paced that it kept me engaged! On the opposite spectrum, being in basic algebra the teacher would explain the same simple concept over and over, with rote problem practice was torturously hard to stay focused because the work was so simple.

And that’s where we get to the part explaining why I think of my ADHD as a superpower, and why if you have it, or your kids have it, or your spouse has it… the key to dealing with it is understanding how to harness the way our brains work.

Learning to Thrive with ADHD

Disclaimer : What follows is NOT medical advice, nor is it necessarily 100% accurate. This is my personal experience and how I’ve come to understand my brain via working with my therapist and talking with other people with ADHD.

A Warp Speed Brain

To have ADHD means that your brain is an engine that’s constantly running at high speed. It basically never stops wanting to process information at a high rate. The “attention” part is just an observable set of behaviors when an ADHD person is understimulated. This is also part of why I now openly associate as hyperactive — my brain is hyperactive! It’s constantly on warp speed and won’t go any other speed.

For instance, one of the hardest things for me to do is fill out a paper check. It’s simple, it’s obvious, there is nothing to solve, it just needs to be filled out. By the time I have started writing the first stroke of the first character, my mind is thinking about things that I need to think about. I’m considering what to have for dinner, then I’m thinking about a movie I want to see, then I come up with an email to send — all in a second. 

I have to haullll myself out of my alternate universe and back to the task at hand and, like a person hanging on the leash of a horse that’s bolting, I’m struggling to just write out the name of the person who I’m writing the check to! This is why ADHD people tend to have terrible handwriting, we’re not able to just only think about moving the pen, we’re in 1,000 different universes.

On the other hand, this entire blog post was written in less than an hour and all in one sitting. I’m having to think through a thousand aspects all at once. My dialog: “Is this too personal? Maybe you should put a warning about this being a personal discussion? Maybe I shouldn’t share this? Oh, the next section should be about working. Should I keep writing more of these?”

And because there is so much to think through and consider for a public leader like myself to write such a personal post, it’s highly engaging! My engine can run at full speed. I haven’t stood up for the entire hour, and I haven’t engaged in other nervous habits I have like picking things up — I haven’t done any of it! 

This is what’s called hyperfocus, and it’s the part of ADHD that can make us potentially far more productive than our peers. I’ve almost arranged my whole life around making sure that I can get myself into hyperfocus as reliably as possible.

Harnessing What My Brain Is Built For

Slow-moving meetings are very difficult for me, but chatting in 20 different chat rooms at the same time on 20 different subjects is very easy for me — so you’ll much more likely see me in chat rooms than scheduling additional meetings. Knowing what my brain is built for helps me organize my schedule, work, and commitments that I sign up for to make sure that I can be as productive as possible.

If you haven’t seen the movie “Everything Everywhere All At Once,” and you are ADHD or love someone who is, you should immediately go watch it! The first time I saw it, I loved it, but I had no idea that one of its writers was diagnosed with ADHD as an adult , and decided to write a sci-fi movie about an ADHD person! The moment I read that it was about having ADHD my heart exploded. It resonated so much with me and it all made sense.

Practically, the only real action in the movie is a woman who needs to file her taxes. Now, don’t get me wrong — it’s a universe-tripping adventure that is incredibly exciting, but if you even take a step back and look at it, really, she was just trying to do her taxes.

But, she has a superpower of being able to travel into universes and be… everywhere all at once. Which is exactly how it feels to be in my mind — my brain is zooming around the universe and it’s visiting different thoughts and ideas and emotions. And if you can learn how to wield that as a power, albeit one that requires careful handling, you can do things that most people would never be able to do!

Co-workers have often positively noted that I see solutions that others miss and I’m able to find a course of action that takes account of multiple possibilities when the future is uncertain (I call it being quantum brained). Those two attributes have led me to create groundbreaking new technologies and build large teams with great open cultures and help solve problems and think strategically. 

It took me until I was 39 to realize that ADHD isn’t something that I had to overcome to have the career I’ve had — it’s been my superpower .

Published Jul 15, 2022

Features 2 comments

Our clinical and medical experts , ranging from licensed therapists and counselors to psychiatric nurse practitioners, author our content, in partnership with our editorial team. In addition, we only use authoritative, trusted, and current sources. This ensures we provide valuable resources to our readers. Read our editorial policy for more information.

Thriveworks was established in 2008, with the ultimate goal of helping people live happy and successful lives. We are clinician-founded and clinician-led. In addition to providing exceptional clinical care and customer service, we accomplish our mission by offering important information about mental health and self-improvement.

We are dedicated to providing you with valuable resources that educate and empower you to live better. First, our content is authored by the experts — our editorial team co-writes our content with mental health professionals at Thriveworks, including therapists, psychiatric nurse practitioners, and more.

We also enforce a tiered review process in which at least three individuals — two or more being licensed clinical experts — review, edit, and approve each piece of content before it is published. Finally, we frequently update old content to reflect the most up-to-date information.

Young white man browsing on his phone instead of working

ADHD Awareness Month: Understanding, advocating, and making an impact

Woman in a denim shirt smiling at her therapist as they discuss ADHD

Expert ADHD therapy services at Thriveworks: Empowering you to thrive

Young professional woman at her desk working in an office

ADHD in women: What are differences in symptoms and diagnoses between men and women?

Want to talk to an ADHD counselor? We have over 2,000 providers across the US ready to help you in person or online.

Hampton Catlin

Hampton Lintorn-Catlin

Discover more

Struggling with ADHD?

Thriveworks can help..

Browse top-rated therapists near you, and find one who meets your needs. We accept most insurances, and offer weekend and evening sessions.

essay on attention deficit disorder

Rated 4.5 from over 14,610 Google reviews

Woman at a desk resting head in hand

The information on this page is not intended to replace assistance, diagnosis, or treatment from a clinical or medical professional. Readers are urged to seek professional help if they are struggling with a mental health condition or another health concern.

If you’re in a crisis, do not use this site. Please call the Suicide & Crisis Lifeline at 988 or use these resources to get immediate help.

essay on attention deficit disorder

Celebrating 25 Years

  • Join ADDitude
  •  | 

Subscribe to Additude Magazine

  • What Is ADHD?
  • The ADHD Brain
  • ADHD Symptoms
  • ADHD in Children
  • ADHD in Adults
  • ADHD in Women
  • Find ADHD Specialists
  • New! Symptom Checker
  • ADHD Symptom Tests
  • All Symptom Tests
  • More in Mental Health
  • Medication Reviews
  • ADHD Medications
  • Natural Remedies
  • ADHD Therapies
  • Managing Treatment
  • Treating Your Child
  • Behavior & Discipline
  • School & Learning
  • Teens with ADHD
  • Positive Parenting
  • Schedules & Routines
  • Organizing Your Child
  • Health & Nutrition
  • More on ADHD Parenting
  • Do I Have ADD?
  • Getting Things Done
  • Relationships
  • Time & Productivity
  • Organization
  • Health & Nutrition
  • More for ADHD Adults
  • Free Webinars
  • Free Downloads
  • ADHD Videos
  • ADHD Directory
  • eBooks + More
  • Newsletters
  • Guest Blogs
  • News & Research
  • For Clinicians
  • For Educators
  • Manage My Subscription
  • Get Back Issues
  • Digital Magazine
  • Gift Subscription
  • Renew My Subscription
  • ADHD Parenting

How to Remove Hurdles to Writing for Students with ADHD

Half of all kids with adhd struggle with writing, which can make every assignment — from straightforward worksheets to full-length essays — feel like torture. boost your child’s skills with these 18 strategies for school and home..

Chris Zeigler Dendy, M.S.

Studies suggest that more than half of children with attention deficit disorder ( ADHD or ADD ) struggle with writing. These students may have an overflow of creative ideas , but often struggle when it comes to getting these ideas onto paper.

Children with ADHD have a hard time getting started — and following through — on writing assignments because they have difficulty picking essay topics, locating appropriate resources, holding and manipulating information in their memory, organizing and sequencing the material, and getting it down on paper — all before they forget what they wanted to say.

But these hurdles don’t have to stop them from writing. Discuss the following ADHD writing strategies with your child’s teacher so you can work together to ease the difficulties attention deficit children have with writing.

Solutions in the Classroom: Guide the Writing Process

—Set up a note system. Ask the student to write her notes about a topic on individual sticky notes. She can then group the notes together that feature similar ideas so she’ll be able to easily identify the major concepts of the subject from the groupings.

—Start small and build skills. Ask students with ADHD to write a paragraph consisting of only two or three sentences. As their skills improve, the students can start writing several paragraphs at a time.

[ Free Download: 18 Writing Tricks for Students with ADHD ]

—Demonstrate essay writing. With the use of an overhead projector, write a paragraph or an entire essay in front of the class, explaining what you are doing at each step. Students can assist you by contributing sentences as you go. Students with ADHD are often visual learners , and tend to do better when they see the teacher work on a task.

—Give writing prompts. Students with ADHD usually don’t generate as many essay ideas as their peers. Help the children with ADHD increase their options for essay assignments by collecting materials that stimulate choices. Read a poem, tell a story, show pictures in magazines, newspapers, or books.

If the student is still struggling to get started, help him by sitting down and talking about the assignment with him. Review his notes from the brainstorming session and ask, “What are some ways you could write the first sentence?” If he doesn’t have an answer, say, “Here’s an idea. How would you write that in your own words?”

—Encourage colorful description. Students with ADHD often have difficulty “dressing up” their written words. Help them add adjectives and use stronger, more active verbs in sentences.

[ How Teens with Learning Differences Can Defeat Writing Challenges ]

—Explain the editing process. Students with ADHD have a hard time writing to length and often produce essays that are too short and lacking in details. Explain how the use of adjectives and adverbs can enhance their composition. Show them how to use a thesaurus, too.

Solutions in the Classroom: Use Accommodations Where Necessary

—Allow enough time. Students with ADHD, especially those with the inattentive subtype, may take longer to process information and should receive extended time to complete assignments.

—Don’t grade early work. Sensitive students are discouraged by negative feedback as they are developing their writing skills. Wait until the paper is finished before assigning it a grade.

—Don’t deduct points for poor handwriting or bad grammar. Unless an assignment is specifically measuring handwriting and grammar skills, when a child is working hard to remember and communicate, let some things slide.

—Use a graphic organizer. A graphic organizer organizes material visually in order to help with memory recall. Distribute pre-printed blank essay forms that students with ADHD can fill in, so they’ll reserve their efforts for the most important task — writing the essay.

—Grade limited essay elements. To encourage writing mastery and avoid overwhelming students, grade only one or two elements at any given time. For example, “This week, I’m grading subject-verb agreement in sentences.” Tighter grading focus channels students’ attention to one or two writing concepts at a time.

Solutions at Home

—Encourage journals. Have your child write down his thoughts about outings to the movies, visits with relatives, or trips to museums. Add some fun to the activity by asking your child to e-mail you his thoughts or text-message you from his cell phone.

—Assist with essay topic selection. Children with ADHD have difficulty narrowing down choices and making decisions. Help your student by listening to all of his ideas and writing down three or four of his strongest topics on cards. Next, review the ideas with him and have him eliminate each topic, one by one – until only the winner is left.

—Brainstorm. Once the topic is identified, ask him for all the ideas he thinks might be related to it. Write the ideas on sticky notes, so he can cluster them together into groupings that will later become paragraphs. He can also cut and paste the ideas into a logical sequence on the computer.

—Stock up on books, movies, games. These materials will introduce new vocabulary words and stimulate thinking. Explore these with your child and ask him questions about them to solicit his views.

—Be your child’s “scribe.” Before your child loses his idea for the great American novel, or for his next English assignment, have him dictate his thoughts to you as you write them out by hand or type them into the computer. As his skills improve over time, he’ll need less of your involvement in this process.

—Go digital. Children with ADHD often write slower than their classmates. Encourage your child to start the writing process on a computer. This way, she’ll keep her work organized and won’t misplace her essay before it’s finished. Also, by working on the computer she can easily rearrange the order of sentences and paragraphs in a second draft.

—Remind your child to proofread. Let your child know that he’ll be able to catch errors if he proofreads his rough draft before handing it in.

High-Tech Writing Helpers for Kids with ADHD

Portable word processor

These battery-operated devices look like a computer keyboard with a small calculator screen. Light and durable, portable word processors can be used at school for note-taking and writing assignments. Back home, files can be transferred to a PC or Mac. Basic models cost about $20.

Speech-recognition software

essay on attention deficit disorder

Word-prediction software

Software such as Co:Writer Solo ($325) helps with spelling and builds vocabulary, providing a drop-down list of words from which a student can choose. It also fills in words to speed composition. Some programs read sentences aloud, so the writer can hear what he has written and catch mistakes as they occur.

Electronic spell-checkers and dictionaries

Enter a word phonetically, and these portable gadgets define the word and provide the correct spelling. Talking devices read the words aloud. Franklin Electronics offers models beginning at about $20.

[ The Common Problems that Lead to Writer’s Block ]

Chris Zeigler Dendy, M.S., is a member of ADDitude’s  ADHD Medical Review Panel .

Learning Challenges: Read These Next

Gwen Stefani of No Doubt

Famous People with Dyslexia, Dyscalculia & Other Learning Differences

Students Raising Hands

9 Things I Wish the World Knew About My Students’ ADHD

Flat classroom with young woman teacher and schoolchildren hand up. Concept businesswoman and students characters at work, school relationship. Vector illustration.

A Teacher’s Guide to NVLD: How to Support Students with Nonverbal Learning Disability

"ADDitude Top 25 Webinars" text with emblem and banner. Pink background.

Top Webinars in ADDitude's History

Adhd newsletter, success @ school, strategies for homework, accommodations, ieps, working with school & more..

It appears JavaScript is disabled in your browser. Please enable JavaScript and refresh the page in order to complete this form.

  • Our Mission

Writing Strategies for Students With ADHD

Here are six challenges and solutions, based on task simplicity and clear instruction, for helping students with ADHD develop their essay-writing skills.

Boy in deep concentration writing with pencil

Too often, students with ADHD (attention deficit hyperactivity disorder) get labeled as "problem students." They often get shuffled into special education programs even if they show no signs of developmental disability. Though these students' brains do work differently, studies prove that it doesn't preclude them from being highly intelligent. That means teachers should pay special attention to help students with ADHD discover their potential and deal with the challenges they face in their learning process.

As essay writing is both the most common and the most complicated assignment for students, writing instruction for students with ADHD requires special efforts. Each step of writing process may present certain difficulties for these young people. Here are some practical solutions for teachers to encourage, motivate, and focus their students on writing process.

1. Difficulty Concentrating on Assignment

Research proves that ADHD doesn’t result in less intelligence, but rather in difficulties controlling emotions, staying motivated, and organizing the thoughts. So a teacher's first task is teaching students focus enough on a writing assignment.

Solution: Give clear, concise instructions.

When assigning an essay or other writing project, be specific and clear about what you expect. Don't leave a lot of room for interpretation. Instead of the assignment "Write about a joyous moment," include instructions in your writing prompt, such as:

  • Think about the last time you felt happy and joyful.
  • Describe the reasons for your happiness.
  • What exactly made you feel joy?
  • What can that feeling be compared to?

Make sure every student knows that he or she should come to you directly with any questions. Plan to take extra time reviewing the instructions with students one to one, writing down short instructions along the way.

2. Difficulty Organizing Thoughts on Paper

Several studies have found that students with ADHD struggle with organizing their thoughts and mental recall. These students can often speak well and explain their thoughts orally, but not in writing.

Solution: Get them organized from the start.

Start each project with a simple note system. Give students the freedom to take their own notes and review them together if possible. Have students pay special attention to filing these notes in a large binder, folder, or other method for making storage and retrieval simple.

To help students understand how to organize their written thoughts, teach them mind mapping . A semantic mind map for an essay may include major nouns, verbs, and adjectives, as well as phrases to use in writing each paragraph. Some introductory and transition sentences will also come in handy. Another step after mind mapping is advanced outlining . Begin and end the initial outline with the words "Intro" and "Conclusion" as placeholders. Then have students expand that outline on their own.

3. Difficulty With Sustained Work on a Single Task

ADHD can make it difficult for students to focus on long-term goals, leading to poor attention and concentration when the task requires work for an extended period of time.

Solution: Create small, manageable milestones.

Since accomplishing a five-page essay takes a lot of time, you can chop it into smaller, easier-to-manage pieces that can be worked on in rotation. Each piece may be checked separately if time allows. Treating every issue and section as an independent task will prevent students from feeling overwhelmed as they work toward a larger goal.

4. Difficulty in Meeting Deadlines

Deadlines are the things that discourage students with ADHD, as they work on assignments more slowly than their classmates, are often distracted, and tend to procrastinate.

Solution: Allow for procrastination.

It may sound ridiculous, but build procrastination into the writing process by breaking up the work and allowing for extra research, brainstorming, and other activities which diversify students' work while still focusing on the end result.

5. Spelling Issues

Students with ADHD often have difficulties with writing, especially in terms of spelling. The most common issues are reversing or omitting letters, words, or phrases. Students may spell the same word differently within the same essay. That's why lots of attention should be paid to spelling.

Solution: Encourage spell checkers, dictionaries, and thesaurus.

There are plenty of writing apps and tools available to check spelling and grammar. As a teacher, you can introduce several apps and let students choose which ones work better for writing essays. When checking the submitted papers and grading the work, highlight the spelling mistakes so that students can pay special attention to the misspelled words and remember the correct variant.

6. Final Editing Issues

Students with ADHD may experience problems during the final editing of their work since, by this time, they will have read and reviewed it several times and may not be paying attention to mistakes.

Solution: Teach them to review their writing step by step.

Take an essay template as an example and show students how to revise it. Go through the editing process slowly, explaining the "why" behind certain changes, especially when it comes to grammatical issues. Assign students the task of revising each other's essays so that when they revise their own final draft, they'll know what to pay attention to and what common mistakes to look for.

Addressing the challenges unique to students with ADHD will help these students find ways to handle their condition effectively and even use it to their advantage. Their unique perspective can be channeled into creative writing, finding new solutions to problems, and most of all, finding, reaching, and even exceeding their goals and fulfilling their full potential.

U.S. flag

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

  • Publications
  • Account settings
  • Advanced Search
  • Journal List

Logo of jpersmed

ADHD: Reviewing the Causes and Evaluating Solutions

Luis núñez-jaramillo.

1 División de Ciencias de la Salud, Universidad de Quintana Roo, Chetumal 77039, Quintana Roo, Mexico; xm.ude.oorqu@zenunl

Andrea Herrera-Solís

2 Laboratorio Efectos Terapéuticos de los Canabinoides, Subdirección de Investigación Biomédica, Hospital General Dr. Manuel Gea González, Calz. de Tlalpan 4800, Belisario Domínguez Secc 16, Tlalpan 14080, Ciudad de México, Mexico; moc.liamg@shaerdnaard

Wendy Verónica Herrera-Morales

Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder in which patients present inattention, hyperactivity, and impulsivity. The etiology of this condition is diverse, including environmental factors and the presence of variants of some genes. However, a great diversity exists among patients regarding the presence of these ADHD-associated factors. Moreover, there are variations in the reported neurophysiological correlates of ADHD. ADHD is often treated pharmacologically, producing an improvement in symptomatology, albeit there are patients who are refractory to the main pharmacological treatments or present side effects to these drugs, highlighting the importance of developing other therapeutic options. Different non-pharmacological treatments are in this review addressed, finding diverse results regarding efficacy. Altogether, ADHD is associated with different etiologies, all of them producing changes in brain development, leading to the characteristic symptomatology of this condition. Given the heterogeneous etiology of ADHD, discussion is presented about the convenience of personalizing ADHD treatment, whether pharmacological or non-pharmacological, to reach an optimum effect in the majority of patients. Approaches to personalizing both pharmacological therapy and neurofeedback are presented.

1. Introduction

Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder (NDD) presenting with inattention, hyperactivity, and impulsivity. It can be classified in three subtypes, depending on the intensity of the symptoms: predominantly inattentive, predominantly hyperactive–impulsive, and combined [ 1 , 2 ]. ADHD has a global prevalence of 5.9% to 7.1% in children and 1.2% to 7.3% in adults [ 3 ].

While most studies address ADHD in children from 7 to 17 years old, it is important to outline that this condition is also present in adults. It has been proposed that the number of adults with ADHD has increased over the last 20 years. A part of this increase is due to the permanence of ADHD symptoms in the adult age in 76% of diagnosed patients. ADHD implies important challenges for academic, personal, and job performance [ 4 ].

As for any other condition affecting brain function, in order to find an adequate treatment for ADHD, it is important to first understand its physiological basis. As with other NDDs, the causes of ADHD are aberrant neural development, affecting neurogenesis, synaptogenesis, myelination, and neuronal and glial proliferation and migration. Even though symptoms begin to appear in childhood, neuronal development is affected from early embryogenesis [ 5 ].

The etiology of ADHD is diverse—gestational, perinatal, and genetic factors have been associated with ADHD incidence. However, each patient presents only a few of them.

2. Environmental Factors Associated with ADHD

The incidence of ADHD is associated with a number of environmental factors during different stages of central nervous system (CNS) development, such as gestational and perinatal periods. In this section, we will address some of the environmental factors that have been associated with ADHD.

2.1. Preconceptional, Gestational, and Perinatal Conditions

Premature birth is an important risk factor for ADHD, since it has been reported that it occurs 2.6 to 4 times more frequently in babies born with low weight or very low weight. Premature birth is associated with alterations in neurogenesis and cell death [ 6 ], and these are in turn associated with reduced cortical expansion, as reported in ADHD patients [ 7 ]. One possible reason for increased risk of developing ADHD in preterm children is inflammation; an increase in inflammation-related molecules is associated with increased risk of developing ADHD symptoms [ 8 ].

Perinatal hypoxia is an environmental factor that increases the risk of developing AHDH, probably due to its effects on dopaminergic transmission and neurotropic signaling [ 9 ].

The intake of nutrients during gestation is very important for proper brain development. An important element during neural development is the polyunsaturated fatty acid docosahexaenoic acid (DHA), promoting proliferation and neural differentiation of neural progenitor cells. Decreased levels of DHA during brain development have been associated with ADHD and other neurodevelopmental disorders [ 10 ], and decreased levels of serum DHA levels have been reported in adult ADHD patients [ 11 ]. Additionally, malnutrition or immune activation in the pregnant mother is a risk factor for ADHD and other neurodevelopmental disorders [ 12 ]. High sucrose consumption during pregnancy is possibly related with ADHD incidence. A study performed on rats reported that high sucrose intake in pregnant rats led to the appearance of ADHD-like symptoms in the offspring, who showed increased locomotor activity, decreased attention, and increased impulsivity. Furthermore, the offspring also presented increased dopamine transporter (DAT) and a decrease in dopamine receptors and mRNA expression in the striatum [ 13 ].

Interestingly, there is evidence in a rat model of the influence of preconceptional conditions on ADHD incidence. Offspring of Female rats administered with ethanol for 8 weeks before mating presented ADHD-like symptoms such as hyperlocomotive activity, impulsivity, and attention deficit. These rats also presented low levels of striatal DAT and increased presence of norepinephrine transporter (NET) in the frontal cortex [ 14 ]. A later work by this group revealed that paternal preconceptional alcohol exposure also produced ADHD-like symptoms in the offspring, presenting decreased expression of DAT mRNA and DAT protein in the cortex and striatum. Furthermore, authors report epigenetic changes in both the sperm of these alcohol-exposed male rats and in the frontal cortex and striatum of the offspring, presenting increased methylation in a CpG region of DAT gene promoter, which is in agreement with the reduced expression of DAT in the offspring [ 15 ].

Another environmental factor associated with ADHD is pesticide exposure during development. A study addressing the issue, both at experimental and epidemiological levels, reported that exposure to the pesticide deltamethrin during gestation and lactation in rats led to ADHD-like symptoms, such as working memory and attention deficits, hyperactivity, and impulsive-like behavior. It also produced increased presence of DAT and D1 receptor in the striatum, as well as increased dopamine release and increased presence of D1 dopamine receptor in the nucleus accumbens. Interestingly, the authors also performed an epidemiological study in humans, revealing that children (6 to 15 years old) with detectable levels of pyrethroid metabolites in urine had more than twice the probability of being diagnosed with ADHD [ 16 ].

2.2. Heavy Metal Exposure

One of the most reported environmental factors associated with ADHD is exposure to neurotoxic heavy metals. A study performed on school children revealed that children (6–7 years old) with ADHD presented higher levels of salivary mercury. However, when including all age groups studied (12–13 years and 15–16 years), no significant correlation was found between increased salivary mercury and ADHD, although a mild tendency was observed [ 17 ].

In the case of manganese, both too high and too low blood levels are associated with cognitive deficits. High concentration of manganese in blood is associated with deficits in thinking, reading, and calculations, as well as with lower learning quotient (indicative of learning disability) and more errors in the continuous performance test (measuring attention and response inhibition). Conversely, low blood level of manganese is associated with a poorer performance in the Stroop test, which is used to assess cognitive inhibition [ 18 ]. Similarly, a study addressing the relationship between manganese in drinking water and ADHD found a higher risk of developing this condition (inattentive but not combined subtype) as exposure to manganese in drinking water increased [ 19 ]. However, a study on manganese in children’s deciduous teeth failed to find an association between this metal and cognitive deficits [ 20 ].

The presence of lead in children’s deciduous teeth is positively associated with hyperactivity or impulsivity, as well as inattention and oppositional or defiant disorder [ 20 ]. A study on children from a lead-contaminated region reported that blood levels of cadmium, lead, and manganese correlated with conduct problems and antisocial behavior [ 21 ]. Another work found a higher concentration of blood lead in ADHD children, which was correlated with hyperactivity–impulsivity symptoms but not with inattention [ 22 , 23 ]. Both genetic [ 24 ] and epigenetic [ 25 ] factors have been reported to contribute to lead-related pathogenesis of ADHD. Moreover, a study carried out in Argentina found that children with high blood concentrations of lead are more likely to develop ADHD [ 26 ].

A review on the effects of prenatal and childhood metal exposure on cognition found suggestive evidence of a relation between cadmium exposure and impaired cognitive ability in children. They did not find evidence of a relationship between cadmium exposure and ADHD [ 27 ]. A more recent study addressing cadmium exposure during pregnancy revealed that a higher blood cadmium concentration during pregnancy is associated with higher scores in ADHD diagnostic tests in female children at 6 years of age, but not in the case of male children [ 28 ].

A recently published work reported that ADHD children present higher urine concentrations of chromium, manganese, cobalt, nickel, copper, molybdenum, tin, barium, and lead [ 29 ]. A recent study analyzing serum concentrations of different metals in ADHD children reported low levels of chromium, manganese, and zinc, as well as increased copper/zinc ratios in these children [ 30 ]. A meta-analysis on the relation between blood and hair zinc and ADHD found no statistical difference between ADHD and control children [ 31 ].

Thus, there are a number of environmental factors associated with ADHD incidence. While environmental factors are not found in all ADHD cases, the data reviewed herein highlight the importance of environment in different developmental stages—and even before conception—in regard to the risk of developing ADHD.

3. Sleep Disorders and ADHD

Sleep deprivation, either acute or chronic, produces decreased cognitive functioning (one of the main traits of ADHD). Interestingly, it also produces the externalizing symptoms observed in ADHD patients. For example, a very tired child might become hyperactive, while in a sleepy adult in a condition where it is not possible to sleep (for example, while driving), the externalizing behavior will help them to remain awake. Thus, both of the core ADHD symptoms can be produced by sleep deprivation. Conversely, hyperactivity in children or high internal activity in adults in the evening might lead to sleep disruption [ 32 ].

Among the sleep disorders found in ADHD patients are delayed sleep phase disorders, insomnia, sleep-disordered breathing, increased motor activity during the night, sleep anxiety, clenching teeth, periodic limb movement, restless legs, increased sleep onset latency and shorter sleep time, night awakenings, narcolepsy, and parasomnias [ 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ]. Among them, delayed sleep phase disorder is one of the most frequently found, being present in 73–78% of both ADHD children and adults. This condition consists of a delay between the sleep propensity cycle and the circadian cycle, leading to increased daytime sleepiness and decreased cognitive functioning [ 32 ].

Sleep disturbance have an impact on daytime vigilance, producing excessive sleepiness [ 32 , 37 , 39 ], and can exacerbate inattention, impulsivity, and hyperactivity as means to remain awake [ 32 , 37 ]. Additionally, stimulant medication might also cause sleep disturbances, although OROS methylphenidate produces less adverse effects on sleep [ 34 , 36 ]. LDX, a stimulant prodrug that undergoes hydrolysis in the bloodstream releasing d-amphetamine, and atomoxetine, a non-stimulant pharmacological treatment for ADHD, do not produce adverse effects on sleep [ 36 ].

Sleep disturbances in ADHD patients can produce significant impairments in attention, mood, and behavior [ 32 , 35 ]. Physiologically, there is evidence supporting an overlap between brain centers regulating sleep and those regulating attention and arousal, so it is possible that affectation of one of these systems also affects the other. Similarly, affectation of noradrenergic and dopaminergic pathways is found in both ADHD and sleep disturbances [ 40 ].

Conversely, during wake time, sleep disturbances produces symptoms resembling those observed in ADHD patients [ 35 , 41 , 42 ]. It is, thus, recommended to assess sleep disorders in patients with ADHD symptoms in order to avoid misdiagnosis [ 41 , 42 ].

The relationship between sleep disorders and ADHD is complex. While ADHD might produce sleep disorders, they could also be coincident conditions [ 36 ]. Moreover, sleep disorders have been proposed to be not only one of the intrinsic features of ADHD, but also might be one of its causes [ 32 , 36 ]. Another possible explanation for this interaction would be an underlying common neurological disease leading to both sleep disorders ad ADHD [ 36 ]. A recent review on the subject proposed that chronic sleep disorders are some of the main causes of ADHD symptoms [ 32 ]. The authors suggested that patients presenting ADHD symptoms should undergo quantification of sleep and sleep problems in order to rule them out as the sole cause of ADHD symptoms. Thus, ADHD treatment should address both the symptoms (with classic ADHD treatment) and the sleep problem [ 32 , 34 , 35 , 36 ], although the effect of this combined treatment still requires further research [ 32 ].

4. Genetic Factors Associated with ADHD

Different studies have revealed an important genetic influence in the etiology of ADHD [ 43 ]. It is a polygenic condition with an important number of genes involved, as confirmed by a genome-wide association study on ADHD reporting 12 significant loci associated with this condition [ 44 ]. Many of the genes reported to be associated with ADHD participate in processes such as neurotransmission, neuritogenesis, synaptogenesis, or receptor location in synapses [ 45 ]. In this review, we will focus on two genes, a neurotrophin (brain-derived neurotrophic factor –BDNF-) and a molecule involved in dopaminergic signaling (DAT).

Brain-derived neurotrophic factor (BDNF) is a neurotrophin with high expression in the brain that is highly concentrated in the hippocampus and cortex. It has an important role in neuronal development, being important for neuronal proliferation, migration, differentiation, and maturation, as well as for synaptogenesis [ 46 ].

BDNF has been implied in ADHD pathophysiology. It has been proposed that low levels of this neurotrophin may explain the reduction in brain volume observed in ADHD patients, and it has also been implied in dopaminergic system homeostasis. Some pharmacological treatments for ADHD promote the regulation of plasma BDNF levels [ 47 ].

4.1.1. Circulating BDNF

Since BDNF is able to cross the blood–brain barrier and plasma concentrations of BDNF are highly correlated with its levels on cerebrospinal fluid, a number of studies have searched for a difference in plasma concentrations of BDNF in ADHD patients when compared against controls. There are reports indicating a lower concentration of BDNF in plasma of ADHD patients, both in children [ 48 ] and adults [ 49 ]. In another study involving children, an increase in plasma BDNF was observed after 6 weeks of treatment with an effective dose of methylphenidate [ 50 ]. In accordance, a recent study revealed that methylphenidate treatment produces an increase in serum BDNF in boys with ADHD [ 51 ]. However, this has not always been replicated, since there are also articles reporting no difference in serum BDNF between children with ADHD and controls [ 52 , 53 , 54 ].

A recently published meta-analysis encompassing studies comparing BDNF levels in ADHD patients without any other comorbidity found no overall difference between ADHD patients and controls. However, when analyzing males and females separately, they found significantly higher levels of plasma BDNF in males with AHDH than in control males, while no difference was found between females with and without ADHD [ 55 ].

Thus, different and even contrary results have been obtained regarding BDNF concentrations in plasma or sera of ADHD patients. While this suggests that the link between BDNF and ADHD is not completely clear, other alternatives should be considered. For example, fluctuations in serum BDNF concentrations in morning and evening samples have been reported [ 56 ], meaning the lack of relation between peripheral BDNF concentration and ADHD might be due to the time of the day when the sample was obtained.

4.1.2. Genetics of BDNF

There are a number single nucleotide polymorphisms (SNP) of the BDNF gene that have been associated with ADHD. Among the most studied variations in the BDNF gene, there is a polymorphism called Val66Met (also known as rs6265), in which a change in codon 66 produces a substitution of the original amino acid (valine) by methionine. The anatomical effects of this variation are more apparent in the hippocampus and cortex [ 46 ]. While some studies have assessed the presence of this SNP in ADHD patients [ 57 , 58 , 59 ], other studies failed to find an association between this polymorphism and ADHD [ 46 , 60 , 61 , 62 , 63 ].

Another SNP of the BDNF gene whose association with ADHD is not conclusive is rs2030324, since some studies report an association between this polymorphism and ADHD [ 57 , 58 , 59 , 64 ], while other reports fail to find this association [ 46 , 60 , 61 , 62 , 63 ].

There are other SNPs of the BDNF gene that have been studied so far, with positive correlations being shown between ADHD and the presence of C270T (rs27656701) [ 58 , 61 ], rs11030101 [ 62 , 64 , 65 ], and rs10835210 [ 62 , 63 ]. There are also reports addressing SNPs of the BDNF gene for which no association with ADHD has been found, including rs12291186, rs7103411 [ 63 ], and rs7103873 [ 62 , 63 ].

Moreover, rare single nucleotide variants of BDNF gen have also been associated with a higher risk of developing ADHD [ 66 ]. However, this is an area that requires further research.

As observed with peripheral BDNF concentrations, genetic variants of the BDNF gene have been associated with ADHD in numerous cases, although in some cases there are contradictory results in different articles (see Table 1 ). Moreover, some of the genetic variants of the BDNF gene associated with ADHD have also been studied in association with other neurological conditions and treatments. For example, C270T is reported to be associated with intellectual disabilities [ 58 ]. Moreover, rs11030101 is associated with a better response to electroconvulsive shock therapy for treatment-resistant depression [ 67 ], with body weight gain in schizophrenic patients treated with atypical antipsychotics [ 68 ], as well as with the presence of major depressive disorder [ 69 ], schizophrenia, and bipolar disorder [ 70 ], although there is another publication in which no evidence of association between this SNP and bipolar disorder was found [ 71 ]. Additionally, rs10835210 has been associated with bipolar disorder, schizophrenia [ 70 ], and phobic disorders [ 72 ].

Polymorphisms of the BDNF gene studied in relation with ADHD incidence. * Polymorphisms for which contradictory results have been reported. rs, reference SNP ID number.

For rs6265 (Val66Met), there are many articles addressing the association of this SNP with different conditions, and in some of them it has been found. For example, some articles report an association of this SNP with major depressive disorder [ 69 , 73 ], while other studies fail to find this association [ 74 , 75 ]. An association has also been reported between rs6265 and amnestic mild cognitive impairment, as well as with the transition from this condition to Alzheimer’s disease [ 76 ]. However, in patients with early-stage breast cancer, this SNP is associated with a lower probability of presenting cognitive impairment after chemotherapy [ 77 ].

4.1.3. Other Neurotrophines

While BDNF has been widely studied in association with ADHD, it is not the only neurotrophin studied in relation with this condition, given the important role of neurotrophines in central nervous system development and synaptic plasticity. In this regard, there are studies addressing the participation of fibroblast growth factor (FGF), vascular endothelial growth factor, insulin-like growth factor (IGF2) [ 47 ], glial-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and neurotrophin-3 (NTF-3) [ 47 , 53 ] in ADHD pathophysiology.

BDNF is a molecule highly involved in synaptic plasticity and has an undisputed role in central nervous system development. Therefore, it is not surprising to find a number of studies associating alterations in the presence of this neurotrophin in serum, or different SNPs of its gene, with ADHD. However, its role in ADHD development is not a constant for every sample of ADHD patients studied so far, and for many of the aspects of this molecule (serum levels, SNPs) there are reports indicating associations, with others finding no association at all. This does not mean that the alterations associated with this molecule are not important for ADHD, but rather highlight the variable etiology of this condition.

4.2. Dopaminergic System

The dopaminergic system emerges in early stages of CNS embryonic development, and an imbalance in this system might affect brain development. It is related with cell proliferation, neuronal differentiation and migration, synaptogenesis, and neurogenesis. Thus, it is not surprising that a role of this neurotransmitter system has been reported in different neurological diseases, including ADHD [ 78 ].

One of the most studied molecules of the dopaminergic system in relation to ADHD is DAT, a molecule responsible for dopamine reuptake, and the main target of two commonly used pharmacological treatments for ADHD, methylphenidate and amphetamines [ 78 ]. Genetic studies support the importance of this neurotransmission system for ADHD. Mice heterozygous for the DAT gene (+/− heterozygotes) are reported to present altered attentional function [ 79 , 80 ] and hyperactivity [ 80 ], while rat models with this heterozygous genotype do not present major affectations [ 81 , 82 ]. However, DAT knockout rats present hyperactivity [ 81 , 82 ], as well as a dysregulation in frontostriatal BDNF function [ 82 ]. Hyperactivity in these rats can be counteracted by amphetamine, haloperidol, and methylphenidate [ 82 ].

In humans, ADHD patients present lower DAT availability in the basal ganglia, caudate nucleus, and putamen [ 83 ]. The DAT gene presents a variable tandem repeat region (VNTR) at the untranslated 3′region, and there are different alleles for this VNTR, with the 9-repeat and 10-repeat alleles being the most frequently encountered. The reported effects of this VNTR on DAT expression vary in different articles, however the most recent results indicate that the 9-repeat allele is associated with a higher DAT expression than the 10-repeat allele. [ 84 ]. The possible association between this VNTR and ADHD has been addressed in various studies. For example, an analysis of both patients and the literature found an association of the 10-repeat/10-repeat genotype with ADHD only in adolescents [ 85 ], studies performed in children reported an association between the 10-repeat/10-repeat genotype and ADHD [ 86 , 87 ], while a recently published meta-analysis reported an association of the 10-repeat allele with ADHD in children and adolescents, specifically in European population [ 88 ]. However, there are also reports indicating no association at all between ADHD and the VNTR of DAT gene (9-repeat/10-repeat, 10-repeat/10-repeat, and 10-repeat/11-repeat genotypes) [ 89 ], no association between the 10-repeat/10-repeat allele with ADHD [ 90 ], and no association between ADHD and the 9-repeat or the 10-repeat alleles for this polymorphism [ 91 ]. The last three studies were performed in children.

Additionally, the relevance of this VNTR has been studied in relation to cognitive function in healthy subjects. Again, mixed results were found. A meta-analysis published in 2016 addressing studies performed in healthy subjects did not find any association between DAT VNTR and different cognitive functions, such as executive functions, inhibition, attention, and long-term declarative memory [ 92 ]. A study performed in children aged 3 to 5 years old addressing the presence of the 9-repeats and 10-repeats alleles revealed that the presence of the 10-repeat allele of the DAT gene is associated with diminished ability to voluntarily regulate reactivity in healthy children [ 93 ]. A recent study on both ADHD and healthy children reported an effect of the specific genotype in the performance of children on attentional switching when studying the whole research sample, in which children carrying the 9-repeat allele performed worse than those carrying the 10-reapet homozygous or the 10-repeat/11-repeat heterozygous allele [ 91 ]

The participation of the dopaminergic system in the pathophysiology of ADHD has been widely reported [ 78 ]. Herein, we study a particular variation of the DAT gene, a VNTR in the 3′ region of the gene, finding articles supporting a role of this polymorphism in ADHD, as well as works failing to find an association between this VNTR and ADHD. This does not imply a lack of importance of this variation, but rather highlights the variability in the genetic etiology of this condition. Moreover, while the dopaminergic system is highly involved in the pathophysiology of ADHD, given its role in CNS development, it is also strongly related with other neuropsychiatric conditions, such as autism [ 78 , 94 , 95 ] and schizophrenia [ 78 , 94 , 96 , 97 ].

5. Changes in Brain Structure and Function in ADHD Patients

As an NDD, ADHD involves alterations of mechanisms such as neurogenesis and synaptogenesis. There are a number of possible mechanisms through which these alterations take place, both environmental and genetic, some of which have been mentioned in the present review. In the end, all of these altered mechanisms produce an altered brain function affecting attention and impulse control, functions regulated by the central nervous system. Understanding the changes in brain function associated with ADHD might shed some light not only on the functional causes of this condition, but also on possible ways to deal with it.

5.1. Brain Imaging Studies

Children with ADHD present atypical connectivity in reward circuitry when compared with control children. Increased connectivity of the nucleus accumbens with the prefrontal cortex was observed to be associated with greater impulsivity [ 98 ].

Hypofunction and abnormal cortico-striatal pathways of the cortico-striato-thalamo-cortical (CSTC) circuit are associated with ADHD. Five different CSTC circuits have been reported: the sustained attention circuit, emotion circuit, selective attention circuit, hyperactivity circuit, and impulsivity–compulsivity circuit. Four of them (except emotion circuit) have been related with ADHD diagnostic criteria. However, pathogenesis of the emotion circuit is also related with ADHD [ 99 ]

A study on ADHD children reported significantly decreased white matter volume, as well as decreased volume in the cortex and caudate nucleus, although it did not reach statistical significance. Cortical thickness was reduced in ADHD patients bilaterally in the frontal cortex and in the right cingulate cortex, structures related with executive function and attention. Regarding default mode network, functional connectivity was reduced in ADHD children in the anterior and posterior cingulate cortexes, lateral prefrontal cortex, left precuneus, and thalamus. However, connectivity was increased in the bilateral posterior medial frontal cortex [ 100 ].

A study on male adolescents with ADHD and controls reported decreased gray matter volume in the left anterior cingulate cortex and bilateral decreases in the occipital cortex, hippocampus–amygdala complex, and cerebellum in ADHD adolescents [ 101 ]. Such decreases in cerebellar volume have been previously reported in both female and male ADHD patients [ 102 ].

An important issue with many of the imaging studies in ADHD patients has been small sample size. A large-scale study performed on children, adolescents, and adults with ADHD reported decreased surface area in children, mainly in the frontal, cingulate, and temporal regions. This effect was more pronounced in younger children (4–9 years old). Moreover, cortical thickness in ADHD children is also reduced in the fusiform gyrus and temporal lobe, an effect more prominent in children of 10 and 11 years old. No change in surface area or cortical thickness was observed in adolescent or adult ADHD patients [ 103 ].

There are important changes in brain morphology in ADHD patients. An elegant study performed in ADHD patients and controls from 6 to 28 years of age analyzed differences in neurodevelopmental trajectories. This study reported that ADHD patients present overall reduced cortical volume, mainly in frontal lobes, and primarily due to a decrease in surface area and gyrification. Interestingly, although both groups presented maturational changes due to age, they presented different trajectories for these changes, suggesting that ADHD is associated with developmentally persistent changes in the whole cortex, mostly due to decreased surface expansion (reduced surface area and less convolution) [ 7 ].

When comparing children with comorbid epilepsy and ADHD with control children, a widespread decrease in cortical thickness is observed, along with decreased volume in some subcortical structures and the brainstem. These alterations were observed early in the course of epilepsy, thus the authors suggested that neurodevelopmental changes occurred before epilepsy onset [ 104 ]. In children with comorbid autism spectrum disorder and ADHD, when compared with typically developing controls, presented significantly lower volumes in left postcentral gyrus. This was observed through magnetic resonance imaging in both children and preadolescents, but was absent in adolescents. The authors suggested that pathophysiology in these comorbid patients may be related to somatosensory deficits and delayed maturation in this area [ 105 ].

5.2. Quantitative Electroencephalography

All these changes lead to alterations in brain function. A frequently used technique for the study of brain activity is quantitative electroencephalography (qEEG), since it has a low cost, a high temporal resolution, and does not need special facilities to be performed. Furthermore, qEEG has also been used to determine the effects of pharmacological treatments on brain activity in order to assess effectiveness [ 106 , 107 ], to choose the correct pharmacological option for a patient [ 108 ], to study the effects of previous pharmacological treatments on the current one [ 109 , 110 ], as well as to determine a possible cognitive effect of the chosen pharmacological treatment [ 111 ].

During the last decades, several studies have performed qEEG analyses on ADHD patients. A review on the subject published in 2012 addressed the main associations between brain activity and ADHD, including increased frontocentral theta activity. Another frequently reported factor, although not always replicated, is an increased theta/beta ratio. For beta and alpha bands, most of the reports have indicated decreased activity, although there are also reports that have indicated increased activity in these frequency bands in ADHD patients [ 112 ]. One of the most used indicators for ADHD is the theta/beta ratio in the Cz region. It has been reported that ADHD children (inattentive and combined subtypes) present increased theta/beta ratios [ 1 ]. Another study found that children with ADHD presented more delta and theta activity [ 113 ]. However, some authors have mentioned that this measure is not necessarily useful for diagnosis, since among other issues, it presents variations according to age [ 114 ].

Another example of the influence of age on brain electrical activity associated with ADHD is a study comparing children with and without ADHD, as well as adults with and without ADHD. Interestingly, children with ADHD presented higher delta and theta activity than control children, while in adults no difference was found between ADHD group and controls in the frequency bands analyzed [ 115 ]. Among the few differences in qEEG activity found in adults with ADHD is a higher gamma activity (39.25–48 Hz), suggesting a functional alteration in dorsal attention network [ 116 ].

ADHD patients often present comorbidities [ 117 ], which might influence qEEG in a different way to the findings in ADHD only patients. For example, children with ADHD and problematic Internet use present differences in qEEG when compared to ADHD only patients. However, no differences were found between ADHD only patients and ADHD patients with depression [ 118 ]. Another study found that adolescents with ADHD and Internet gaming disorder presented lower relative delta power and greater relative beta power than adolescents with ADHD only [ 119 ].

It is noteworthy that although a number of studies have been published regarding neurophysiological correlates of ADHD through qEEG, there are still some differences in the results reported by different authors. Beyond possible methodological differences, there are a number of factors reported to influence qEEG activity in ADHD patients, which might be responsible—at least in part—for the differences reported so far, and which might be of importance when using qEEG information to choose or design a therapeutic approach. These factors include comorbidities [ 4 , 120 ] and the ages of the patients [ 114 , 116 , 121 ]. Other factors reported to affect qEEG activity in other populations and conditions are ethnicity [ 122 , 123 , 124 , 125 , 126 ], sociocultural environment during development [ 127 , 128 ], and the degree of advancement of a psychiatric condition, as reported for alcohol dependence [ 129 , 130 , 131 ].

6. Therapeutic Approaches

6.1. pharmacological treatment.

Both stimulant and non-stimulant pharmacological treatments have proven to be effective in diminishing ADHD symptoms in children and adolescents [ 132 , 133 ], although stimulant medication seems to have greater effectiveness [ 133 , 134 ]. Herein, we will address one frequently used stimulant (methylphenidate) and one frequently used non-stimulant (atomoxetine)

6.1.1. Methylphenidate

Methylphenidate is one of the most used drugs for ADHD treatment. It has been present in the market for 50 years and it reduces excessive hyperactivity, impulsivity, and inattention in children and adolescents with ADHD. In the United States, it is prescribed to 8% of children and adolescents under 15 years of age and to around 3% to 5% of the same population in Europe [ 135 ].

Methylphenidate blocks DAT and NET, reducing reuptake and producing an increase in available dopamine and norepinephrine in the synaptic cleft [ 135 , 136 , 137 ], leading to increased dopamine and norepinephrine transmission in the prefrontal cortex [ 132 ]. A meta-analysis on the effects of methylphenidate treatment on ADHD in adults found it effective in improving neurocognitive performance, accomplishing better results than placebo groups in terms of working memory, reaction time variability, vigilance, driving, and response inhibition [ 136 ].

6.1.2. Atomoxetine

Atomoxetine has been reported to be effective for ADHD treatment [ 138 ], being more effective in adults than in children [ 134 ].

Atomoxetine blocks norepinephrine reuptake, producing increased presence of norepinephrine and dopamine in prefrontal cortex [ 132 ]. Since atomoxetine does not produce an increase of dopamine or norepinephrine in the nucleus accumbens, it lacks abuse potential [ 132 , 139 ]. This drug is associated with improvements in quality of life in children adolescents and adults, although this parameter is not further increased with long-term use [ 139 ].

6.1.3. Adverse Effects

Both stimulant and non-stimulant pharmacological treatments for ADHD produce adverse effects in a percentage of treated patients. The main adverse effects found for these drugs (% of patients treated with stimulants/% of patients treated with non-stimulants) are decreased appetite (28.6%/14.2%), nausea (7.9%/10.3%), headache (14.5%/20.8%), insomnia (12.3%/8.6%), nasopharyngitis (6.0%/7.1%), dizziness (5.1%/10.0%), abdominal pain (7.8%/11.5%), irritability (9.3%/6.9%), and somnolence (4.4%/34.1%) [ 133 ].

A systematic review on the adverse effects of methylphenidate in children and adolescents revealed that about 1 in 100 patients present serious adverse events after methylphenidate treatment (including death, cardiac problems and psychiatric disorders), while more than half of the patients treated with methylphenidate suffer one or more adverse events. The authors concluded that it is important to identify subgroups of patients who might be harmed by methylphenidate treatment and highlight the importance of remaining alert to possible adverse events in patients with this treatment [ 135 ]. There might also be uncommon adverse effects. For example, there is a report of 3 cases of systemic sclerosis associated with methylphenidate treatment [ 140 ]. The authors of the last study suggested that patients with signs of autoimmune or vasospastic conditions should be briefed about this possible side effect before commencing methylphenidate treatment.

A systematic review on possible adverse effects of atomoxetine, including decreased growth rate, cardiovascular and hepatic effects, aggression, psychosis, seizures, and suicidal ideation, determined that evidence indicates it is safe to use in ADHD patients [ 141 ]. Furthermore, the presence of comorbidities does not interfere with treatment efficacy, nor does treatment exacerbate comorbid symptoms [ 142 , 143 ]. However, it is important to be alert to other possible adverse effects. A case report and review indicated that the appearance of tics is a common side effect of atomoxetine treatment [ 144 ].

Methylphenidate and atomoxetine are known to increase heart rate and blood pressure, raising concern regarding possible cardiovascular effects of these drugs in ADHD patients. A review on the cardiovascular effects of these drugs in healthy subjects found the drug to be safe to use. Most of these studies were performed in children and adolescents, although there have also been some studies performed on adults, with no serious risk being reported in these subjects either. However, patient blood pressure and heart rate should be monitored on a regular basis. Moreover, careful follow-up should be performed for patients presenting certain cardiovascular conditions [ 145 ].

Weight loss has also been reported after atomoxetine treatment, occurring during the first two years of treatment. However, evidence suggests this decrease begins to be compensated between 2 and 5 years after the beginning of treatment [ 141 ]. Similarly, methylphenidate has been associated with adverse effects such as anorexia, weight loss, and insomnia [ 146 ].

A comparative study on short-term effects of methylphenidate and atomoxetine on ADHD reported significantly higher weight loss in children treated with atomoxetine [ 147 ]. However, a more recent study reported that children present significantly more weight loss after methylphenidate than after atomoxetine treatment [ 148 ].

A meta-analysis on gastrointestinal adverse effects of methylphenidate reported increased risk of decreased appetite, weight loss, and abdominal pain in children and adolescents under this pharmacological treatment [ 149 ].

A comparison between the presence of adverse effects after methylphenidate and atomoxetine treatments in ADHD children indicated methylphenidate as a safer option, since children under atomoxetine treatment presented higher incidence rates of anorexia, nausea, somnolence, dizziness, and vomiting than children under methylphenidate treatment [ 147 ]. A more recent study reported similar results, since children treated with atomoxetine presented higher incidence rates of mild adverse effects, such as decreased appetite, weight loss, dyspepsia, abdominal pain, stomach ache, irritability, mood disorders, and dizziness. As for severe adverse effects, patients under atomoxetine treatment presented higher incidence rates of gastrointestinal, neuropsychiatric, and cardiovascular effects [ 150 ].

6.1.4. Long-Term Adverse Effects

Long-term adverse effects of methylphenidate are the subject of intense study, given that it is the first-line stimulant drug used for ADHD treatment in children, adolescents, and adults [ 11 , 151 ]. A review on the subject addressed different adverse effects studied in patients after long-term (over one year) administration of methylphenidate, including low mood or depression, anxiety, irritability or emotional reactivity, suicidal behavior or ideation, bipolar disorder, psychotic symptoms, substance use disorders, tics, seizures or EEG abnormalities, and sleep disorders. The authors concluded that existing information indicates that methylphenidate is safe to use, although caution should be taken when prescribing this drug to specific groups, such as preschool children, patients prone to psychosis or tics, and high-risk adolescents [ 152 ]. However, the need for more studies on the long-term effects of treatment with this drug is highlighted, since studies in humans are rather scarce and with a high degree of heterogeneity in terms of methodological approach [ 151 , 152 ].

6.1.5. Long-Term Therapeutic Effect

Given that ADHD is a chronic disorder and that many of the children presenting ADHD will still present symptoms in adulthood, it is particularly important to determine the long-term effectiveness of pharmacological treatments. However, very few studies address this issue, and no conclusion can yet be drawn regarding the long-term effects (years) of pharmacological treatment of ADHD on symptom reduction and quality of life. Thus, the long-term efficacy of drug treatment for ADHD remains under debate [ 153 , 154 , 155 , 156 ]

Current pharmacological treatments for ADHD have proven to be safe and effective. The efficacy of these treatments on ADHD symptoms is clear, and thus pharmacological therapy is often used to treat ADHD patients [ 136 , 138 , 141 , 152 ]. However, there are also some drawbacks to this therapeutic approach, including the time required to reach the effective dose for each patient [ 3 , 157 ]; the lack of response in some patients [ 121 , 158 , 159 , 160 ]; the unresolved issue of long-term effectiveness (of great importance given that in many cases the treatment must go on for years) [ 153 , 154 , 155 , 156 ]; the presence of adverse effects, which although not life threatening in most cases, are nevertheless upsetting [ 133 , 135 , 144 ]; and the existence of specific groups of patients with whom a greater caution must be taken [ 140 , 145 , 152 ]. Altogether, these drawbacks have led to the search of new therapeutic approaches. One of the strategies studied so far is the possibility of using other drugs to treat ADHD, including drugs interacting with serotoninergic (metadoxine, paroxetine, duloxetine, buspirone), glutamatergic (memantine), cholinergic (AZD3480, AZD1446, lobeline, galantamine, mecamylamine), histaminergic (mk-0249), and catecholaminergic neurotransmission systems (modafinil, droxidopa, desipramine, bupropion, nomifensine, reboxetine, venlafaxine, duloxetine, guanfacine, aripiprazol, dasotraline, selegiline), as well as lithium [ 161 ].

6.2. Non-Pharmacological Therapies

Pharmacological therapy is effective although presents some inconveniences, including the existence of adverse effects in some patients and lack of effect in others. Therefore, there are also different non-pharmacological approaches for ADHD treatment.

6.2.1. Behavioral Parent Training

The goal of parent training is to equip parents with techniques that will be useful in managing ADHD-related behavior presented by their children. A systematic review published on 2011 found no reliable effect of ADHD children’s behavior, although it may lead to increased confidence and decreased stress in parents [ 162 ]. Later studies found an effect of behavioral parent training on ADHD symptoms, which is not increased by previous working memory training, although this combination did produce positive effects on working memory storage and processing [ 163 ]. It is noteworthy that cognitive functioning of both parents and children influences the effectiveness of this therapeutic approach on ADHD symptoms. Better working memory in children and higher parental response caution presented an association with improvements in inattention. As for conduct problems, better parental self-regulation was associated with a better result in this area. However, none of the measured cognitive functions in children or parents were associated with improvements in hyperactivity [ 164 ]. Moreover, behavioral parent training improves coexistence at home, since a reduction in the frequency and severity of problematic situations is produced, along with a reduction of stress in parents [ 165 ].

6.2.2. Cognitive Behavioral Therapy

Cognitive behavioral therapy (CBT) has also been used to treat ADHD. A review performed on the subject found CBT to be effective in reducing ADHD symptoms in adults, however only when improvement was evaluated by the patient and not when evaluated by the clinician [ 166 ], although a more recent meta-analysis on the subject reported a good effect of CBT on ADHD adults [ 167 ]. A Cochrane systematic review concluded that CBT has a positive effect on ADHD symptoms, either alone or in conjunction with other therapies, although considered the evidence to be low-quality in accordance with the Grading of Recommendations Assessment, Development and Evaluation (GRADE) working group approach. [ 168 ]. A meta-analysis found that CBT is one of the most effective non-pharmacological options to treat ADHD, ranking just after physical exercise [ 169 ]. A later systematic review confirmed the effects of CBT on ADHD symptoms [ 170 ]. A recent study reported CBT to be effective in reducing ADHD symptoms in patients, either with or without conjunct medication [ 171 ].

6.2.3. Attention Training Techniques

Attention training techniques are often used to improve life quality and increase well-being. Given the effect of these techniques on brain activity, as well as on attention and self-regulation, their use to reduce ADHD symptoms and improve life quality in these patients is currently under study [ 172 ].

Mindfulness can be defined as paying attention to the present, an activity that implies sustained attention. A systematic review on the effects of mindfulness-based interventions on ADHD found that such approaches were popular among adults with ADHD, finding improvements in attention, although the effects of such approaches in children and adolescents are still unclear [ 173 ]. A recent meta-review reported a large effect size of mindfulness on ADHD [ 174 ]. A review on the effects of mindfulness-based cognitive therapy on ADHD adults reported good effects of this therapeutic approach, especially when used in conjunction with pharmacological therapy [ 175 ], while a systematic review analyzing the effects of meditation-based techniques (either on parents and children or on children only) on ADHD children could not draw a clear conclusion regarding beneficial effects [ 176 ].

Adult ADHD patients that underwent an 8-week mindfulness awareness practice period presented decreased ADHD, depression, and anxiety symptoms [ 177 ]. Similarly, a study performed with children revealed that an 8-week period of mindfulness-oriented meditation produced improvements in the performance of neuropsychological tests, as well as in ADHD symptoms. Although encouraging, the authors stated that the results are still preliminary, given the small number of children participating in the study [ 178 ]. There are also results indicating that this technique produces an improvement in ADHD symptoms in ADHD children with oppositional defiant disorder [ 179 ].

6.2.4. Neurofeedback

Neurofeedback (NFB) is a therapy in which patients learn to modify EEG patterns through operant conditioning. There are articles reporting the induction of plastic changes after NFB training [ 180 , 181 , 182 , 183 ], supporting a theory explaining the effects of NFB on different brain disorders through the induction of synaptic plasticity, leading to an homeostatic set point. Additionally, besides some unusual cases of headache, no collateral effects have been reported with this technique. One of the most interesting aspects of NFB is the induction of plastic changes from within the brain under normal physiological conditions, without the need for an external stimuli such as pharmacological treatments or transcranial stimulation to alter brain activity, thus the probability of adverse effects is minimal [ 181 ].

Specific NFB protocols have been developed over the decades. These protocols were designed based on articles reporting specific qEEG variations in neurological patients or qEEG patterns associated with cognitive function. Some of these standardized protocols have been studied in terms of their ability to treat ADHD [ 184 ].

Several articles have addressed the use of NFB in ADHD patients. The results have been mixed and numerous meta-analyses have been published on the subject. The conclusions of these meta-analyses have also been mixed. There are meta-analyses reporting good effects of NFB on ADHD [ 185 , 186 , 187 ], not finding reliable effects [ 188 ], not reaching a conclusion on the subject of efficacy [ 189 ], finding a minor effect of this therapeutic approach significantly below what is observed with pharmacological treatment [ 190 ], or finding a minor effect only in the presence of pharmacological treatment [ 191 ].

An overview of recent publications gave the same impression. Some reports found effects of NFB theta/beta or theta/alpha protocols on ADHD, measurable at follow-up 8 weeks or 12 months after treatment completion [ 192 , 193 ]. Other reports found no effect [ 194 , 195 , 196 ]. Moreover, there are reports revealing a minor effect of NFB, below the effect levels of other therapeutic approaches [ 197 , 198 , 199 ].

NFB is a therapeutic approach widely studied for ADHD treatment. The results so far have been mixed. However, given the absence of side effects and its ability to induce synaptic plasticity [ 181 ], it is an option worth keeping in mind.

6.2.5. Other Non-Pharmacological Approaches

The use of non-pharmacological supplementations, such as polyunsaturated fatty acids, peptides, amino acids, plat extracts, probiotics, micronutrients, and herbal supplementation, is currently being studied in order to determine their usefulness in treating ADHD. However, further research is still needed in this area [ 200 ].

A study performed in ADHD children under methylphenidate treatment for whom zinc supplementation was added reported no significant effect of zinc supplementation on the total score for a parent’s questionnaire for ADHD or in the hyperactivity and impulsivity subscales. However, zinc-supplemented children present improvements in inattention scores [ 201 ].

A meta-analysis on non-pharmacological interventions for ADHD patients found that physical exercise produced a good effect on ADHD cognitive symptoms, especially aerobic exercise targeting executive functions [ 169 ].

7. Treatment Personalization

In the first sections of this review, we addressed some of the factors associated with ADHD incidence, ranging from a variety of environmental factors to the presence of different genetic polymorphisms. However, these different etiologies are not always present, since patients might present one or another (see Section 2 and Section 3 ). Similarly, while there are some changes in brain activity associated with ADHD, they are not always the same (see Section 4 ). Accordingly, there is also variation in the response of patients to both pharmacological and non-pharmacological treatments (see Section 5 ).

Since the etiology of ADHD could be very different from patient to patient, the precise nature of the physiological changes underlying the clinical manifestations of ADHD in each case could be slightly different, affecting the effectiveness of the chosen treatment and possibly explaining the variation in the effect of the same treatment on different patients. This can be observed in the variations in qEEG activity observed in different studies [ 112 , 113 , 114 , 116 , 121 ]. However, the design of personalized treatments based on specific characteristics of each patient could lead to better clinical results. In this regard, strategies to adjust therapeutic approaches based on patients’ characteristics have been used for both pharmacological and non-pharmacological therapies.

Selecting the appropriate pharmacological treatment and the dose to be used takes some time, given the large inter-individual variability regarding treatment efficacy, leading to a delay in reaching a therapeutic effect, and in some cases producing an early termination of treatment due to frustration, either by the provider or the family [ 157 ]. Moreover, there is some variability regarding patient response to methylphenidate, including patients that do not achieve adequate symptom control or experience adverse effects with commonly used doses. Therefore, dose optimization has been proposed as a means to achieve an adequate effect for most of the patients, enhancing both the efficacy and safety of methylphenidate treatment [ 3 ]. This has led to the search for strategies to find adequate treatments for each patient, such as pharmacogenomics, in which a patient’s genotype for a particular gene is used to predict the effects of medication in that patient. However, in spite of the progress that has already been made, no pharmacogenomic test so far has been found to be helpful in treatment selection [ 157 ].

Treatment resistance has been reported for both atomoxetine [ 158 ] and methylphenidate [ 121 , 159 , 160 ]. For this reason, qEEG can be used as a source of information to determine at an earlier point whether methylphenidate [ 121 , 160 , 202 ] or atomoxetine [ 107 , 202 ] is effective or if an alternative treatment is needed for a patient.

Most of the reports on the use of NFB for ADHD use a standardized protocol, either equal for all participants or adapted to each patients after qEEG analysis. However, there is another more personalized approach known as qEEG-informed (or qEEG-guided) NFB. In this variant of NFB, rather than selecting a particular protocol (for example, theta/beta ratio) and applying it to all participants, subjects receive a NFB protocol selected for them after qEEG analysis. This type of NFB has been successfully used in schizophrenia [ 203 ], obsessive compulsive disorder [ 204 ], migraine [ 205 ], dementia [ 206 ], and with learning-disabled children [ 207 , 208 ].

There are so far only two studies applying qEEG-informed NFB in ADHD patients, so it is not yet possible to perform a meta-analysis on the effects of this type of NFB on ADHD. However, a positive effect of NFB has been reported in both published studies [ 209 , 210 ].

8. Discussion

ADHD is an NDD with a complex etiology. While it is clear that its main cause is alterations in neurodevelopmental processes such as synaptogenesis, myelination, and neurogenesis [ 5 ], the causes of these neurodevelopmental alterations are diverse. In some cases they might be associated with environmental factors such as premature birth [ 6 ], perinatal problems [ 9 ], nutrition during pregnancy [ 10 ], or exposure to heavy metals [ 17 , 18 , 19 , 26 , 27 , 29 ]. Additionally, there is strong evidence of genetic influence on ADHD [ 43 , 44 ], and an interaction between environmental and genetic factors cannot be discarded.

The purpose of this review is not to fully describe all factors associated with ADHD appearance, but rather to address some of the main etiologies described so far, in order to clarify the high diversity of factors associated with this NDD. When analyzing the different sections of this review, one thing becomes evident—that ADHD patients are diverse regarding the etiology of their condition and their responses to treatment. This heterogeneity outlines the high variability in patients’ particular conditions regarding ADHD symptom manifestation and treatment, since it is probable that the underlying neurophysiological alterations for each patient are at least slightly different. Thus, standardized treatment (either pharmacological or non-pharmacological) may not be equally efficient in all cases.

Moreover, there could be other factors that are usually disregarded in relation with ADHD incidence, but which might play an important role in this condition. Recently, the gut microbiome has been the subject of intense research as an ADHD-associated factor, and even though further research is needed in order to determine its precise influence on ADHD, there are already reports indicating a possible link between them [ 211 , 212 , 213 , 214 ].

In the end, all of these factors produce changes in brain structure and function [ 1 , 7 , 112 , 113 , 114 , 115 ], leading to the symptomatology observed in ADHD patients. Therapeutic approaches to treat this condition have the objective of compensating such alterations in order to reduce symptoms and improve quality of life. However, as we have observed in this review, not all patients present the same neurophysiological changes. Studies performed on qEEG activity have yielded different results regarding brain electrical activity in ADHD patients [ 4 , 112 , 114 , 120 ]. Additionally, both brain imaging and qEEG techniques have revealed that changes are not consistent throughout the lifespan, being different in children and adults [ 114 , 115 , 116 , 121 ]. Therefore, there is a need for treatment personalization for each ADHD patient in order to achieve greater effect with minimal adverse effects.

Pharmacological treatments, both stimulants and non-stimulants have proven to be effective and safe for ADHD patients [ 132 , 133 ], and thus are widely prescribed to treat this condition. However, the pharmacological approach to ADHD treatment has some drawbacks, mostly regarding difficulties in reaching effectiveness in all patients [ 3 , 121 , 157 , 158 , 159 , 160 ] and the presence of adverse effects [ 133 , 135 , 144 ].

The search for other therapeutic options has led to the assessment of the effects of other drugs on ADHD [ 161 ], as well as the design of non-pharmacological treatments, such as behavioral parent training, CBT, attention-improving techniques, and NFB.

The effects of behavioral parent training on ADHD symptoms in children are not consistent, with some articles finding effects [ 163 ] and others not finding any [ 162 ]. However, behavioral parent training does reduce stress in parents and promotes a better coexistence at home, which is favorable for children [ 162 , 165 ]. In the case of CBT, there is more evidence indicating a good effect in reducing ADHD symptoms [ 167 , 168 , 169 , 170 , 171 ]

Attention training techniques are still under intense study. There is some evidence regarding the effect of this technique on ADHD in adults [ 173 , 175 ], while in children and adolescents the results are not clear so far [ 173 , 176 ].

A number of studies on the effect of NFB on ADHD symptoms have yielded different results, either finding a positive effect [ 185 , 186 , 187 , 192 , 193 ], a mild effect [ 190 , 197 , 198 , 199 ], or no effect at all [ 188 , 194 , 195 , 196 ]. However, NFB has a number of advantages that encourage the search for an adequate protocol to treat ADHD patients. It is targeted directly to change brain activity associated with the condition under treatment, it has virtually no side effects, and the therapeutic effect is due to the induction of plastic changes in the central nervous system, thus it might establish a long-term changes [ 180 , 181 , 182 , 183 ].

9. Conclusions

In the present review, we have gone through some of the factors associated with ADHD, and it is clear that a great heterogeneity exists in the etiology of this condition. Therapeutic approaches, although functional in many cases, also show heterogeneity in their effects in certain groups of patients. The diverse range of effects of the therapeutic approaches used should not be a surprise, given the diversity of etiologies found in ADHD. Even though clinical manifestations of this condition might be similar (diagnosis is based on the presence certain symptoms), the same clinical manifestations could occur with different underlying physiological changes, considering the variations in qEEG activity in different groups of patients [ 112 , 113 , 114 , 116 , 121 ]. Thus, these neurophysiological changes presented by patients may not necessarily respond in equal form to a given therapeutic approach. Given the inter-personal variance in the etiology of ADHD, it is advisable to personalize the therapeutic approach. Regarding pharmacological therapies, dosage optimization [ 3 ], pharmacogenomics [ 157 ], and the use of qEEG to select the adequate drug for a given patient have been proposed [ 107 , 121 , 160 , 202 ].

Regarding non-pharmacological options, the use of qEEG-informed NFB has been proposed for personalized treatment in ADHD patients. The studies carried out to date have shown positive results [ 209 , 210 ], although the number of studies is still too small to draw a conclusion. However, given the advantages of NFB [ 181 ] and the positive effects of this approach reported for other conditions [ 203 , 204 , 205 , 206 , 207 , 208 ], it is worth performing further studies on the effectiveness of this type of NFB on ADHD.

Author Contributions

Conceptualization, L.N.-J. and W.V.H.-M. writing—reviewing and editing, L.N.-J., W.V.H.-M., and A.H.-S. All authors have read and agreed to the published version of the manuscript.

This research received no external funding

Conflicts of Interest

The authors declare no conflict of interest.

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

  • Undergraduate
  • High School
  • Architecture
  • American History
  • Asian History
  • Antique Literature
  • American Literature
  • Asian Literature
  • Classic English Literature
  • World Literature
  • Creative Writing
  • Linguistics
  • Criminal Justice
  • Legal Issues
  • Anthropology
  • Archaeology
  • Political Science
  • World Affairs
  • African-American Studies
  • East European Studies
  • Latin-American Studies
  • Native-American Studies
  • West European Studies
  • Family and Consumer Science
  • Social Issues
  • Women and Gender Studies
  • Social Work
  • Natural Sciences
  • Pharmacology
  • Earth science
  • Agriculture
  • Agricultural Studies
  • Computer Science
  • IT Management
  • Mathematics
  • Investments
  • Engineering and Technology
  • Engineering
  • Aeronautics
  • Medicine and Health
  • Alternative Medicine
  • Communications and Media
  • Advertising
  • Communication Strategies
  • Public Relations
  • Educational Theories
  • Teacher's Career
  • Chicago/Turabian
  • Company Analysis
  • Education Theories
  • Shakespeare
  • Canadian Studies
  • Food Safety
  • Relation of Global Warming and Extreme Weather Condition
  • Movie Review
  • Admission Essay
  • Annotated Bibliography
  • Application Essay
  • Article Critique
  • Article Review
  • Article Writing
  • Book Review
  • Business Plan
  • Business Proposal
  • Capstone Project
  • Cover Letter
  • Creative Essay
  • Dissertation
  • Dissertation - Abstract
  • Dissertation - Conclusion
  • Dissertation - Discussion
  • Dissertation - Hypothesis
  • Dissertation - Introduction
  • Dissertation - Literature
  • Dissertation - Methodology
  • Dissertation - Results
  • GCSE Coursework
  • Grant Proposal
  • Marketing Plan
  • Multiple Choice Quiz
  • Personal Statement
  • Power Point Presentation
  • Power Point Presentation With Speaker Notes
  • Questionnaire
  • Reaction Paper
  • Research Paper
  • Research Proposal
  • SWOT analysis
  • Thesis Paper
  • Online Quiz
  • Literature Review
  • Movie Analysis
  • Statistics problem
  • Math Problem
  • All papers examples
  • How It Works
  • Money Back Policy
  • Terms of Use
  • Privacy Policy
  • We Are Hiring

Attention-Deficit Hyperactivity Disorder (ADHD), Essay Example

Pages: 3

Words: 922

Hire a Writer for Custom Essay

Use 10% Off Discount: "custom10" in 1 Click 👇

You are free to use it as an inspiration or a source for your own work.

Introduction

Symptoms, Diagnosis and Development

Attention-Deficit Hyperactivity Disorder (ADHD) manifests itself with the symptoms of impulsiveness, inability to focus or concentrate impulsivity and hyperactivity. It is a chronic neurobehavioral syndrome further classified as a psychiatric disorder. Often people diagnosed with this disorder tend to have trouble focusing on situations that require extreme concentration, organization and those of a decisive nature leading doctors and others to believe they are unable to take full responsibility for their efforts. “Statistics show that boys are affected at a rate of five times higher than girls and approximately 2-4% of adults are diagnosed with the deficit.” (“Attention-Deficit Hyperactivity Disorder, 2009”). “Maturation and learning is essential to proper human development. The first twelve years of age are extremely important in the development into adolescent and adulthood years.” (Shaffer & Kipp, 2009).

Particularly in children the inattentiveness is shown through patterns of disorganization at school and at home. Teachers may make comments that the child is not performing well in school because of the inability to focus on the homework or coursework. At home the parents may notice that the child’s behaviour is not very good because he/she may not want to cooperate with simple tasks around the home or the child may appear to be tuning the parents’ out when making a simple request to do your homework or to clean your room. The child may be having issues at day-care and the day-care facility may want to eject the child for what appears to be careless or disruptive behaviour. With respect to adults with ADHD, the adult may be experiencing forgetfulness such as losing things around the house, inability to cooperate with co-worker or showing patterns or disorganization in his/her life. Children and adults may have temper outbursts and aggressive behaviour. Adults may have a pattern of job changing. Symptoms such as restlessness or unable to sit still may be present in both children and adults. Especially in children symptoms of play with loud noise might be present. Symptoms may not appear so readily in a one-on-one focused setting rather may excel in such places as outdoor gatherings such as family gatherings or outside public events.

Development

ADHD has a very profound effect on the academic development of school aged children because the inability to concentrate on their school work. This research is based on eliminating the bias factor associated with improper conduct associated with the disorder. If this factor is added to the disorder the chances of a pre-schooler succeeding in school is dramatically declined. Arranging an environment that is stimuli free is a key to success for an ADHD student. Medication is another useful tool to aid AHDH children; however some parents and doctors do not like to commence medication at such a young and vulnerable age.

Sigmund Freud’s theory of psychosexual behaviour is probably one of the best known as well as the most controversial. Psychosexual energy is the driving force behind the development of a child’s personality. If these stages are completed successfully then a child’s personality will develop normally and if not the child will develop a fixation from the undeveloped stage. The stages are the oral stage, the anal stage, the phallic stage, the latent period and the genital stage.” The downside of Freud’s theory is that is psychologically based on males rather than female development. Future predictions by Freud are rather vague and too vague to predict behaviours from childhood to adulthood.” (Shaffer & Kipp, 2009).

ADHD has a very strong emotional effect on a child. “Often it is noted that children with ADHD are behind in emotional development as compared to other children of their same age. With this in mind the children with ADHD may have problems with relation to social contacts making friends and communicating with others on the same level.” (“How Does ADHD Affect a Child’s Emotional Development?”, 2009). Normal children may be introverted and when they make a friend they keep a friend for life. Children with ADHD appear to be outgoing and friendly but their impulsiveness and hyperactivity actually keeps them from making friends and connecting with others socially.  Through these associations of outbursts and impulses, they isolate themselves from others.

Often it is noted through research that there is a co-existence of ADHD with other disorders such as depression, bi-polar and learning disabilities. Not always though are ADHD patients not able to learn properly. It is through slowing down the stimuli that the child or adult will be able to concentrate enough to learn. The decision on how to do this whether through the use of medication or physically will be determined best by the doctor and/or psychiatrist. Sometimes a combination of both will be used.

Behaviour modification techniques may be essential to the child or adult diagnosed with ADHD. “Providing clear and consistent boundaries and a normal and concise routine is essential to promoting the best performance from an ADHD child and an ADHD adult.” (“Behavioural Techniques for Children with ADHD, 2009”). Set an example for a child with ADHD with your patterns of behaviour and continue to examine your communication patterns as the child matures in age.

[1] Shaffer D & Kipp K (2009) Developmental Psychology: Childhood and Adolescence Retrieved September 20, 2009 from, http://books.google.com/books?id=CuvXxrhk8HUC&pg=PT22&dq=Developmental+Psychology+(Chilhood+%26+Adolenscence)+8th+Edition+(new)&ei=mF22Sp7gEJPSNMW6ubEP#v=onepage&q=&f=false

[1] How Does ADHD Affect a Child’s Emotional Development? (2009) How Does ADHD Affect a Child’s Emotional Development? Retrieved September 19, 2009 from,  http://www.healthcentral.com/adhd/c/question/274929/67783

[1] Attention-Deficit Hyperactivity Disorder (2009) Attention-Deficit Hyperactivity Disorder Retrieved September 19, 2009 from, http://www.neurologychannel.com/adhd/index.shtml

[1] Behavioural Techniques for Children with ADHD (2009) Behavioural Techniques for Children with ADHD Retrieved September 19, 2009 from, http://www.webmd.com/add-adhd/guide/adhd-behavioral-techniques?page=2

Stuck with your Essay?

Get in touch with one of our experts for instant help!

The Job Redesign and Workplace Rewards, Essay Example

Memory Assignment, Essay Example

Time is precious

don’t waste it!

Plagiarism-free guarantee

Privacy guarantee

Secure checkout

Money back guarantee

E-book

Related Essay Samples & Examples

Voting as a civic responsibility, essay example.

Pages: 1

Words: 287

Utilitarianism and Its Applications, Essay Example

Words: 356

The Age-Related Changes of the Older Person, Essay Example

Pages: 2

Words: 448

The Problems ESOL Teachers Face, Essay Example

Pages: 8

Words: 2293

Should English Be the Primary Language? Essay Example

Pages: 4

Words: 999

The Term “Social Construction of Reality”, Essay Example

Words: 371

  • Bipolar Disorder
  • Therapy Center
  • When To See a Therapist
  • Types of Therapy
  • Best Online Therapy
  • Best Couples Therapy
  • Best Family Therapy
  • Managing Stress
  • Sleep and Dreaming
  • Understanding Emotions
  • Self-Improvement
  • Healthy Relationships
  • Student Resources
  • Personality Types
  • Verywell Mind Insights
  • 2023 Verywell Mind 25
  • Mental Health in the Classroom
  • Editorial Process
  • Meet Our Review Board
  • Crisis Support

Writing Problems Common for Students With ADHD

damircudic / E+ / Getty Images

Children with ADHD are more likely to develop writing problems than children without ADHD, regardless of gender. Among both boys and girls with ADHD who also have a reading disability, however, girls have an even higher chance of developing a written language disorder, creating even more challenges for girls in the classroom.  

The Process of Writing Involves Integration of Several Skills

The technique involved in expressing oneself through writing is actually a quite complex, multi-step process. It requires the integration of several skills, including planning, analyzing, and organizing thoughts; prioritizing and sequencing information; remembering and implementing correct spelling, punctuation and grammar rules; as well as fine motor coordination.

As students age and move into high school and college , the expectations around writing become even more demanding. Essays and reports that require students to communicate what they know on paper factor more prominently into the curriculum. It is no wonder that writing can create such anxiety in students with ADHD. Simply starting the process and getting ideas and thoughts out of their head in an organized manner and down on paper can feel like an uphill battle.

Many students with ADHD find that it takes them longer than their classmates to complete their work. And when they do complete their assignments, they may find that they produce less written work—shorter reports, less "discussion" on discussion questions, and fewer sentences on each test question—as compared to their peers without ADHD.

ADHD Challenges That May Lead to Writing Difficulties

Why is it so tough for students with ADHD to produce well-crafted, thoughtful, carefully edited writing? Here are nine of the top reasons:

  • Keeping ideas in mind long enough to remember what one wants to say
  • Maintaining focus on the "train of thought" so the flow of the writing does not veer off course
  • Keeping in mind the big picture of what you want to communicate, while manipulating the ideas, details, and wording
  • With the time and frustration it can take to complete work, there is often no time (or energy) remaining to check over the details, edit assignments, and make corrections.
  • Students with ADHD generally have problems with focus and attention to details, making it likely that they will make errors in spelling, grammar, or punctuation.  
  • If a child is impulsive, they may also rush through schoolwork. As a result, papers are often filled with "careless" mistakes.
  • The whole proofreading and editing process can be quite tedious, so if a student does attempt to review work, they may easily lose interest and focus.
  • Challenges with fine motor coordination can complicate writing ability further. Many students with ADHD labor with their fine motor coordination, resulting in slower, messier penmanship that can be very difficult to read.  
  • Simply sustaining the attention and mental energy required for writing can be a struggle for someone with ADHD.

Students with ADHD can work on strategies to improve writing skills that address common learning problems that can interfere with the expression of written language.

Yoshimasu K, Barbaresi WJ, Colligan RC, et al. Written-Language Disorder Among Children With and Without ADHD in a Population-Based Birth Cohort . Pediatrics . 2011;128(3):e605-612. doi:10.1542/peds.2010-2581

Centers for Disease Control and Prevention. ADHD in the Classroom: Helping Children Succeed in School . Updated September 3, 2020.

Mokobane M, Pillay BJ, Meyer A. Fine motor deficits and attention deficit hyperactivity disorder in primary school children . S Afr J Psychiatr . 2019;25:1232. doi:10.4102/sajpsychiatry.v25i0.1232

Rief SF. How To Reach And Teach Children with ADD / ADHD: Practical Techniques, Strategies, and Interventions . Germany: Wiley; 2012.

Zeigler Dendy CA. Teaching Teens with ADD, ADHD & Executive Function Deficits: A Quick Reference Guide for Teachers and Parents . Maryland: Woodbine House; 2011.

By Keath Low  Keath Low, MA, is a therapist and clinical scientist with the Carolina Institute for Developmental Disabilities at the University of North Carolina. She specializes in treatment of ADD/ADHD.

What is ADHD?

Signs and symptoms.

  • Managing Symptoms

ADHD in Adults

More information.

ADHD is one of the most common neurodevelopmental disorders of childhood. It is usually first diagnosed in childhood and often lasts into adulthood. Children with ADHD may have trouble paying attention, controlling impulsive behaviors (may act without thinking about what the result will be), or be overly active.

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

Learn more about signs and symptoms

CHADD's National Resource Center on ADHD

Get information and support from the National Resource Center on ADHD

There are three different ways ADHD presents itself, depending on which types of symptoms are strongest in the individual:

  • Predominantly Inattentive Presentation: It is hard for the individual to organize or finish a task, to pay attention to details, or to follow instructions or conversations. The person is easily distracted or forgets details of daily routines.
  • Predominantly Hyperactive-Impulsive Presentation: The person fidgets and talks a lot. It is hard to sit still for long (e.g., for a meal or while doing homework). Smaller children may run, jump or climb constantly. The individual feels restless and has trouble with impulsivity. Someone who is impulsive may interrupt others a lot, grab things from people, or speak at inappropriate times. It is hard for the person to wait their turn or listen to directions. A person with impulsiveness may have more accidents and injuries than others.
  • Combined Presentation: Symptoms of the above two types are equally present in the person.

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

 Learn about symptoms of ADHD, how ADHD is diagnosed, and treatment recommendations including behavior therapy, medication, and school support.

Causes of ADHD

Scientists are studying cause(s) and risk factors in an effort to find better ways to manage and reduce the chances of a person having ADHD. The cause(s) and risk factors for ADHD are unknown, but current research shows that genetics plays an important role. Recent studies link genetic factors with ADHD. 1

In addition to genetics, scientists are studying other possible causes and risk factors including:

  • Brain injury
  • Exposure to environmental risks (e.g., lead) during pregnancy or at a young age
  • Alcohol and tobacco use during pregnancy
  • Premature delivery
  • Low birth weight

Research does not support the popularly held views that ADHD is caused by eating too much sugar, watching too much television, parenting, or social and environmental factors such as poverty or family chaos. Of course, many things, including these, might make symptoms worse, especially in certain people. But the evidence is not strong enough to conclude that they are the main causes of ADHD.

ADHD Fact Sheet

Download and Print this fact sheet [PDF – 473 KB]

Deciding if a child has ADHD is a process with several steps. There is no single test to diagnose ADHD, and many other problems, like anxiety, depression, sleep problems, and certain types of learning disabilities, can have similar symptoms. One step of the process involves having a medical exam, including hearing and vision tests , to rule out other problems with symptoms like ADHD. Diagnosing ADHD usually includes a checklist for rating ADHD symptoms and taking a history of the child from parents, teachers, and sometimes, the child.

Learn more about the criteria for diagnosing ADHD

physician speaking to family

In most cases, ADHD is best treated with a combination of behavior therapy and medication. For preschool-aged children (4-5 years of age) with ADHD, behavior therapy, particularly training for parents, is recommended as the first line of treatment before medication is tried. What works best can depend on the child and family. Good treatment plans will include close monitoring, follow-ups, and making changes, if needed, along the way.

Learn more about treatments

Managing Symptoms: Staying Healthy

Being healthy is important for all children and can be especially important for children with ADHD. In addition to behavioral therapy and medication, having a healthy lifestyle can make it easier for your child to deal with ADHD symptoms. Here are some healthy behaviors that may help:

  • Developing healthy eating habits  such as eating plenty of fruits, vegetables, and whole grains and choosing lean protein sources
  • Participating in daily  physical activity based on age
  • Limiting the amount of daily screen time from TVs, computers, phones, and other electronics
  • Getting the recommended amount of sleep each night based on age

If you or your doctor has concerns about ADHD, you can take your child to a specialist such as a child psychologist, child psychiatrist, or developmental pediatrician, or you can contact your local early intervention agency (for children under 3) or public school (for children 3 and older).

The Centers for Disease Control and Prevention (CDC) funds the National Resource Center on ADHD , a program of CHADD – Children and Adults with Attention-Deficit/Hyperactivity Disorder. Their website has links to information for people with ADHD and their families. The National Resource Center operates a call center (1-866-200-8098) with trained staff to answer questions about ADHD.

For more information on services for children with special needs, visit the Center for Parent Information and Resources.  To find the Parent Center near you, you can visit this website.

ADHD can last into adulthood. Some adults have ADHD but have never been diagnosed. The symptoms can cause difficulty at work, at home, or with relationships. Symptoms may look different at older ages, for example, hyperactivity may appear as extreme restlessness. Symptoms can become more severe when the demands of adulthood increase. For more information about diagnosis and treatment throughout the lifespan, please visit the websites of the National Resource Center on ADHD  and the National Institutes of Mental Health .

  • National Resource Center on ADHD
  • National Institute of Mental Health (NIMH)
  • Faraone, S. V., Banaschewski, T., Coghill, D., Zheng, Y., Biederman, J., Bellgrove, M. A., . . . Wang, Y. (2021). The World Federation of ADHD International Consensus Statement: 208 evidence-based conclusions about the disorder. Neuroscience & Biobehavioral Reviews. doi:10.1016/j.neubiorev.2021.01.022

To receive email updates about this topic, enter your email address:

Exit Notification / Disclaimer Policy

  • The Centers for Disease Control and Prevention (CDC) cannot attest to the accuracy of a non-federal website.
  • Linking to a non-federal website does not constitute an endorsement by CDC or any of its employees of the sponsors or the information and products presented on the website.
  • You will be subject to the destination website's privacy policy when you follow the link.
  • CDC is not responsible for Section 508 compliance (accessibility) on other federal or private website.

Attention Deficit Hyperactivity Disorder (ADHD)

Attention Deficit Hyperactivity Disorder (ADHD) is a neurodevelopment disorder that is commonly seen amongst children, characterized by impulsive and hyperactive symptoms that can seriously affect day-to-day functioning. Beyond its obvious symptoms, this disorder affects a child’s academic performance, social interactions, and emotional health, among other aspects of their life. It’s critical to identify the intricacies of ADHD and modify instructional strategies to meet each child’s specific demands. This acknowledgement is especially important in the context of inclusive education, where the goal is to give every student equal chances regardless of their unique disabilities and to create a supportive atmosphere for a range of learning styles.

UNIFEC which is responsible for Children’s rights and responsibilities advocates for inclusive education as a platform for acknowledging and catering to the special needs of children suffering from ADHD (Al-Hroub et al., 2023). In this way we create an environment that values every child’s participation in learning as we all meet their needs. This agrees with UNICEF’s guidelines which states that every child has a right to proper education aimed at their all round development. In the inclusive education scenario, child with ADHD is identified and special attention provided such as creation af an environment that lessens feeling alone and building esteem and personal worth. Ilene Schwartz reiterates in her TEDxEastsidePrep lecture of 2015 that students with different challenges such as ADHD can benefit from inclusive environments and how this can greatly improve their wellbeing. These settings help in the development of a child’s emotions and also satisfies his or her normal academic needs.

Ensuring that children with the ADHD disorder get inclusive education is in line with other laws such as Disability Discrimination Act of 1992, that enhances the importances of inclusive education for people living with disabilities (Kim et al., 2019). This statutory support reinforces the moral requirements that instructors must respect, creating a cohesive environment, breaking barriers and promoting justice. Inclusion education goes beyond following the set standards; It entails developing a caring world where every learner with special needs and disabilities have an opportunity to thrive

The essay will delve deeper into these topics in the sections provided of this research review, highlighting the effects of ADHD on academic achievements, social dynamics and emotional health in inclusive learning environments. It intends to contribute to a thorough understanding of ADHD in the context of inclusive education by exploring pertinent policies and ethical issues.

The Key Issues Affecting Children with Attention Deficit Hyperactivity Disorder

In the landscape of inclusive education, some key issues of ADHD are children frequently experiencing Social issues and stigma. Children with these attributes can be isolated even further and subjected to bully and rejection (Nguyen & Hinshaw, 2020). As such, these children remain aloof from others because of their impulsitivity and hyperactivity. However, these are not just issues of isolation but also affects the feeling of worth and one’s academic achievement It is key developing a school climate that will promote social interaction while at the same time fight stigmatization. The establishment of a nurturing environment becomes imperative in this scenario. It means creating an environment in which all children inclusive of those affected by ADHD get the feeling of respect appreciation and on the same level as their classmates. A pillar in the fight for true educational fairness is the emphasis on inclusivity. Acknowledging and addressing the social difficulties that children with ADHD encounter improves their general wellbeing and advances a more comprehensive and successful inclusive education approach.

Teachers have difficulties in managing classes with students having ADHD. Maintaining a good, conducive environment and checking on disruptive behaviors proves very hard (Vu & Nguyen, 2020). Emphasizing the above highlighted problems, it is evident that educators face enormous challenges in attending to the specific requirements of kids with ADHD which points towards the need for further understanding as well as better means of addressing such problems. In order to create a true inclusive learning environment, one has to develop and implement strategies based on each child’s specific requirements. Parents, special need’s experts, and teachers should work as a team while sharing information regarding inclusive education for children with ADHD. It remains necessary to maintain communication among all parties so that there is recognition of each other’s needs as well as their fulfillment. It is crucial to create appropriate care plans for children with ADHD jointly with families and specialists in the field. Therefore, when facing these roadblocks it is essential that children with ADHD grow up in nurturing an interactional and cooperating educational mileu.

Nevertheless, despite the acknowledged value of cooperation, considerable barriers stand in the way of efficient coordination. Time constraints and miscommunications are noted as the two main obstacles that can prevent the cooperative efforts required for inclusive education. For kids with ADHD to live in a cohesive and encouraging environment, these challenges must be overcome. It becomes essential to cultivate fruitful collaborations if inclusive education is to be truly successful. This calls for removing the obstacles that have been found and fostering an environment that promotes productive cooperation between educators, parents, and special needs experts.

To sum up, creating successful tactics and interventions for ADHD in inclusive education requires a thorough grasp of the major concerns surrounding the disorder. Through acknowledging the social obstacles, managing a classroom effectively, and fostering cooperation and dialogue, educators and legislators can strive to establish inclusive settings that address the varied requirements of kids with ADHD. The knowledge gathered from current literature serves as a basis for establishing an academic stance in favor of inclusive teaching methods that genuinely assist kids with ADHD and enhance their success and general well-being.

Implementing Inclusive Educational Strategies for ADHD: A Multifaceted Approach

The aim is to create a conducive learning environment that comprehensively tackles some of the fundamental ADHD challenges and through incorporating the findings from the study on ADHD into effective teaching strategies. There are some strategies deduced from the text that could lead to an improvement in inclusive education techniques. Promoting understanding as well as, accepting society towards the children with ADHD helps ease the social barriers and discrimination against these children. Adding lessons and activities that promote kindness, tolerance, and appreciation for differences could make schools friendlier places. It follows UNICEF values stressed in the literature that any child must have education promoting their overall growth.

Teachers can also incorporate social skills instruction into the curriculum to give all students—including those with ADHD—the abilities they need to engage with others in a productive way. This strategy is in line with Ilene Schwartz’s TEDx lecture, which highlights the transforming power of inclusive environments in improving students’ general wellbeing—including that of kids with ADHD (Nicholson et al., 2020).The literature indicates that a thorough grasp of ADHD is crucial for managing classes containing children with the disease. Sessions for professional growth for teachers might include topics such as efficient classroom management techniques and understanding of ADHD. This entails taking preemptive measures to deal with potentially disruptive behavior while preserving a friendly and inclusive educational setting. As the literature emphasizes, giving educators the tools and assistance they need guarantees that they can fulfill the special needs of children with ADHD.

Collaboration among educators, parents, and SNEPs is important to ensuring equal educational opportunities for children with ADHD. The research suggests having an articulated communication plan which ensures that a specific requirement is addressed towards every individual at all time. Families and experts in special needs work together to develop customized support for their kids suffering from ADHD. In the same manner, it becomes necessary for them to have a network in the school community. Through workshops and support groups, parents, educators and students should be involved in order to bring about effective communication and cooperative action. Such types of projects are in compliance with acts, such as Disability Discrimination Acts, whereby persons with disabilities must posses equal opportunities when it comes to education.

In summary, putting knowledge into reality in the area of inclusive education for kids with ADHD requires a multimodal strategy that tackles the various issues raised in the literature. Teachers may create an inclusive atmosphere that effectively addresses the social obstacles and stigma that children with ADHD confront by using ideas from a variety of sources. Using specially designed lessons and activities to promote a culture of understanding, empathy, and acceptance is in line with UNICEF’s mission to support the holistic development of every child. Teachers can receive focused professional development to help them manage classrooms inclusively. This will provide them the tools they need to deal with disruptive behaviors head-on and keep the classroom welcoming and inclusive. Providing educators with resources and support ensures they can adequately navigate the unique requirements of children with ADHD, as emphasized in the literature. Consistent communication plans involving teachers, parents, and special needs experts encourage effective collaboration and communication, which are essential components of inclusive education. This cooperative endeavor includes creating care plans that provide customized assistance for kids with ADHD. Putting up workshops and support groups for the school community helps to improve communication and collaboration, which is in line with laws that prioritize providing people with disabilities with equal access to education. Every child, including those with ADHD, may thrive in an inclusive educational environment that acknowledges and celebrates their individual needs and skills thanks to this all-encompassing program.

The comprehensive research review informs targeted inclusive educational approaches in the context of attention deficit hyperactive disorder (ADHD). Through understanding, addressing social issues and class teaching, teachers can create a class atmosphere that promotes, respects children’s different abilities. Cooperation between educators, parents, and experts in special needs education; specialized communication, assistance, tailored for each student. As it is inspired by modern research, this all-encompasing approach shows deep intention in offering each kid identical opportunities and developing learning environment that honours diversity.

Al-Hroub, A., Tilawi, A., & Jouni, N. (2023). Equitable and Inclusive Education in Lebanon: Policies and Practices for Special Needs Learners in Lebanon. In  School Inclusion in Lebanon: Integrating Research on Students with Giftedness and Learning Disabilities into Practice  (pp. 1-24). Cham: Springer International Publishing. https://link.springer.com/chapter/10.1007/978-3-031-34779-5_1

Kim, M., King, M. D., & Jennings, J. (2019). ADHD remission, inclusive special education, and socioeconomic disparities.  SSM-population health ,  8 , 100420. https://www.sciencedirect.com/science/article/pii/S2352827318301046

Nguyen, P. T., & Hinshaw, S. P. (2020). Understanding the stigma associated with ADHD: Hope for the future?.  The ADHD Report ,  28 (5), 1-10. https://guilfordjournals.com/doi/abs/10.1521/adhd.2020.28.5.1

Nicholson, J., Maniates, H., Yee, S., Williams, T., Ufoegbune, V., & Erazo-Chavez, R. (2021).  Principals as early learning leaders: Effectively supporting our youngest learners . Teachers College Press. https://books.google.co.ke/books?hl=en&lr=&id=b89cEAAAQBAJ&oi=fnd&pg=PT11&dq=This+strategy+is+in+line+with+Ilene+Schwartz%27s+TEDx+lecture,+which+highlights+the+transforming+power+of+inclusive+environments+in+improving+students%27+general+wellbeing%E2%80%94including+that+of+kids+with+ADHD&ots=umX5octUHx&sig=3V6n3SHBZH7LjtHW-C_DWpMt5jM&redir_esc=y#v=onepage&q&f=false

Vu, H. H., & Nguyen, N. U. (2020). Classroom management techniques for teaching English inclusively to adhd and asd primary students in Vietnam.  VNU Journal of Foreign Studies ,  36 (3). https://js.vnu.edu.vn/FS/article/view/4556

Cite This Work

To export a reference to this article please select a referencing style below:

Related Essays

Human growth and development through the lifespan, lying in a native and foreign language, political polarization in the usa, comprehensive psychiatric emergency program (cpep), psychological effects of immigration, the american presidency – skowronek essay question, popular essay topics.

  • American Dream
  • Artificial Intelligence
  • Black Lives Matter
  • Bullying Essay
  • Career Goals Essay
  • Causes of the Civil War
  • Child Abusing
  • Civil Rights Movement
  • Community Service
  • Cultural Identity
  • Cyber Bullying
  • Death Penalty
  • Depression Essay
  • Domestic Violence
  • Freedom of Speech
  • Global Warming
  • Gun Control
  • Human Trafficking
  • I Believe Essay
  • Immigration
  • Importance of Education
  • Israel and Palestine Conflict
  • Leadership Essay
  • Legalizing Marijuanas
  • Mental Health
  • National Honor Society
  • Police Brutality
  • Pollution Essay
  • Racism Essay
  • Romeo and Juliet
  • Same Sex Marriages
  • Social Media
  • The Great Gatsby
  • The Yellow Wallpaper
  • Time Management
  • To Kill a Mockingbird
  • Violent Video Games
  • What Makes You Unique
  • Why I Want to Be a Nurse
  • Send us an e-mail
  • U.S. Department of Health & Human Services

National Institutes of Health (NIH) - Turning Discovery into Health

  • Virtual Tour
  • Staff Directory
  • En Español

You are here

News releases.

Media Advisory

Wednesday, March 13, 2024

NIH researchers identify brain connections associated with ADHD in youth

Large study finds atypical interactions between the frontal cortex and information processing centers deep in the brain.

Image showing differences in subcortico-cortical connectivity in youth with and without ADHD.

Researchers at the National Institutes of Health (NIH) have discovered that symptoms of attention-deficit/hyperactivity disorder (ADHD) are tied to atypical interactions between the brain’s frontal cortex and information processing centers deep in the brain. The researchers examined more than 10,000 functional brain images of youth with ADHD and published their results in the American Journal of Psychiatry . The study was led by researchers at NIH’s National Institute of Mental Health (NIMH) and National Human Genome Research Institute.

Luke Norman, Ph.D., a staff scientist in the NIMH Office of the Clinical Director, and colleagues analyzed brain images supplied by more than 8,000 youth with and without ADHD sourced from six different functional imaging datasets. Using these images, the researchers examined associations between functional brain connectivity and ADHD symptoms.

They found that youth with ADHD had heightened connectivity between structures deep in the brain involved in learning, movement, reward, and emotion (caudate, putamen, and nucleus accumbens seeds) and structures in the frontal area of the brain involved in attention and control of unwanted behaviors (superior temporal gyri, insula, inferior parietal lobe, and inferior frontal gyri).

While neuroscience researchers have long suspected that ADHD symptoms result from atypical interactions between the frontal cortex and these deep information-processing brain structures, studies testing this model have returned mixed findings, possibly due to the small nature of the studies, with only 100 or so subjects. Researchers suggest that the smaller studies may not have been able to reliably detect the brain interactions leading to the complex behaviors seen in ADHD.

The findings from this study help further our understanding of the brain processes contributing to ADHD symptoms—information that can help inform clinically relevant research and advancements.

Luke Norman, Ph.D., staff scientist in the NIMH Office of the Clinical Director and lead author of the paper

Norman, L. J., Sudre, G., Price, J., & Shaw, P. (2024). Subcortico-cortical dysconnectivity in ADHD: A voxel-wise mega-analysis across multiple cohorts. American Journal of Psychiatry . https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.20230026

About the National Institute of Mental Health (NIMH): The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery, and cure. For more information, visit the NIMH website .

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov .

NIH…Turning Discovery Into Health ®

Connect with Us

  • More Social Media from NIH

NIMH Logo

Transforming the understanding and treatment of mental illnesses.

Información en español

Celebrating 75 Years! Learn More >>

  • Science News
  • Meetings and Events
  • Social Media
  • Press Resources
  • Email Updates
  • Innovation Speaker Series

NIH Researchers Identify Brain Connections Associated With ADHD in Youth

Large study finds atypical interactions between the frontal cortex and information processing centers deep in the brain

March 13, 2024 • Media Advisory

Researchers at the National Institutes of Health (NIH) have discovered that symptoms of attention-deficit/hyperactivity disorder (ADHD) are tied to atypical interactions between the brain’s frontal cortex and information processing centers deep in the brain. The researchers examined more than 10,000 functional brain images of youth with ADHD and published their results in the American Journal of Psychiatry . The study was led by researchers at NIH’s National Institute of Mental Health (NIMH) and National Human Genome Research Institute.

Luke Norman, Ph.D., a staff scientist in the NIMH Office of the Clinical Director, and colleagues analyzed brain images supplied by more than 8,000 youth with and without ADHD sourced from six different functional imaging datasets. Using these images, the researchers examined associations between functional brain connectivity and ADHD symptoms.

They found that youth with ADHD had heightened connectivity between structures deep in the brain involved in learning, movement, reward, and emotion (caudate, putamen, and nucleus accumbens seeds) and structures in the frontal area of the brain involved in attention and control of unwanted behaviors (superior temporal gyri, insula, inferior parietal lobe, and inferior frontal gyri).

While neuroscience researchers have long suspected that ADHD symptoms result from atypical interactions between the frontal cortex and these deep information-processing brain structures, studies testing this model have returned mixed findings, possibly due to the small nature of the studies, with only 100 or so subjects. Researchers suggest that the smaller studies may not have been able to reliably detect the brain interactions leading to the complex behaviors seen in ADHD.

The findings from this study help further our understanding of the brain processes contributing to ADHD symptoms—information that can help inform clinically relevant research and advancements.

Luke Norman, Ph.D., staff scientist in the NIMH Office of the Clinical Director and lead author of the paper

Norman, L. J., Sudre, G., Price, J., & Shaw, P. (2024). Subcortico-cortical dysconnectivity in ADHD: A voxel-wise mega-analysis across multiple cohorts. American Journal of Psychiatry .  https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.20230026  

About the National Institute of Mental Health (NIMH): The mission of the NIMH  is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the NIMH website .

About the National Institutes of Health (NIH) : NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH  and its programs, visit the NIH website  .

NIH…Turning Discovery Into Health ®

Assessing the Contribution of Measures of Attention and Executive Function to Diagnosis of ADHD or Autism

  • Original Article
  • Published: 13 March 2024

Cite this article

  • Kelsey Harkness   ORCID: orcid.org/0000-0002-5770-9964 1 , 2 , 3 ,
  • Signe Bray 2 , 3 , 5 ,
  • Chelsea M. Durber 4 ,
  • Deborah Dewey 2 , 3 , 5 &
  • Kara Murias 2 , 3 , 5  

36 Accesses

1 Altmetric

Explore all metrics

Attention and executive function (EF) dysregulation are common in a number of disorders including autism and attention-deficit/hyperactivity disorder (ADHD). Better understanding of the relationship between indirect and direct measures of attention and EF and common neurodevelopmental diagnoses may contribute to more efficient and effective diagnostic assessment in childhood. We obtained cognitive (NIH Toolbox, Little Man Task, Matrix Reasoning Task, and Rey Delayed Recall) and symptom (CBCL, and BPMT) assessment data from the Adolescent Brain and Cognitive Development (ABCD) database for three groups, autistic (N = 110), ADHD (N = 878), and control without autism or ADHD diagnoses (N = 9130) and used ridge regression to determine which attention and EF assessments were most strongly associated with autism or ADHD. More variance was accounted for in the model for the ADHD group (31%) compared to the autism group (2.7%). Finally, we ran odds ratios (using clinical cutoffs where available and 2 standard deviations below the mean when not) for each assessment measure, which generally demonstrated a greater significance within the indirect measures when compared to the direct measures. These results add to the growing literature of symptom variably across diagnostic groups allowing for better understanding of presentations in autism and ADHD and how best to assess diagnosis. It also highlights the increased difficulty in differentiating autism and controls when compared to ADHD and controls and the importance of indirect measures of attention and EF in this differentiation.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price includes VAT (Russian Federation)

Instant access to the full article PDF.

Rent this article via DeepDyve

Institutional subscriptions

Abbreviations

Attention-Deficit Hyperactivity Disorder

Adolescent Brain and Cognitive Development

Executive Function

Childhood Behavioral Checklist

Brief Problem Monitoring Teacher Report

Kiddie Score for Affective Disorders and Schizophrenia

Rey Auditory Verbal Learning Test

Achenbach, T.M., and L.A. Rescorla. 2001. (2001). Manual for the ASEBA School-Age Forms & Profiles.University of Vermont, Research Center for Children, Youth, & Families. Burlington

Bonnelle, V., et al. (2011). Default mode network connectivity predicts sustained attention deficits after traumatic brain injury. Journal of Neuroscience, 31 (38), 13442–13451.

Article   CAS   Google Scholar  

Bowler, D. M., Limoges, E., & Mottron, L. (2009). Different verbal learning strategies in Autism spectrum disorder: Evidence from the rey auditory verbal learning test. Journal of Autism and Developmental Disorders, 39 (6), 910–915.

Article   Google Scholar  

Boxhoorn, S., et al. (2018). Attention profiles in autism spectrum disorder and subtypes of attention-deficit/hyperactivity disorder. European Child and Adolescent Psychiatry, 27 (11), 1433–1447. https://doi.org/10.1007/s00787-018-1138-8

Clark, B., & Bélanger, S. A. (2018). ADHD in children and youth: Part 3-assessment and treatment with comorbid ASD, ID, or prematurity. Paediatrics and Child Health (Canada), 23 (7), 485–490.

Dellapiazza, F., et al. (2021). Clinical characteristics of children with ASD and comorbid ADHD: Association with social impairment and externalizing and internalizing behaviours. Research in Developmental Disabilities, 113 (103930), 2023. https://doi.org/10.1016/j.ridd.2021.103930

Dickson, K. S., Suhrheinrich, J., Rieth, S. R., & Stahmer, A. C. (2018). Parent and teacher concordance of child outcomes for youth with Autism spectrum disorder. Journal of Autism and Developmental Disorders, 48 (5), 1423.

Article   PubMed Central   Google Scholar  

Dugbartey, A. T., et al. (1999). WAIS-III matrix reasoning test performance in a mixed clinical sample. Clinical Neuropsychologist, 13 (4), 396–404.

Earle, William James. 2014. “DSM-5.” Philosophical Forum .

Farhat, L. C., et al. (2022). ADHD and Autism symptoms in youth: A network analysis. Journal of Child Psychology and Psychiatry and Allied Disciplines, 63 (2), 143–151.

Article   PubMed   Google Scholar  

Feil, E. G., et al. (2016). Early intervention for preschoolers at risk for attention-deficit/hyperactivity disorder: Preschool first step to success. Behavioral Disorders, 41 (2), 95–106.

Article   PubMed   PubMed Central   Google Scholar  

Gómez-Pérez, M., Mar, M. D., Calero, S. M., & Molinero, C. (2016). Discrepancies between direct and Indirect measures of interpersonal and neurocognitive skills in Autism spectrum disorder children. Journal of Clinical and Experimental Neuropsychology, 38 (8), 875–886. https://doi.org/10.1080/13803395.2016.1170106

Harpin, V., et al. (2016). Long-term outcomes of ADHD: A systematic review of self-esteem and social function. Journal of Attention Disorders, 20 (4), 295–305.

Article   CAS   PubMed   Google Scholar  

Hollingdale, J., et al. (2020). Autistic spectrum disorder symptoms in children and adolescents with attention-deficit/hyperactivity disorder: A meta-analytical review. Psychological Medicine, 50 (13), 2240–2253.

Karcher, N. R., & Barch, D. M. (2021). The ABCD study: Understanding the Development of risk for mental and physical health outcomes. Neuropsychopharmacology, 46 (1), 131–142. https://doi.org/10.1038/s41386-020-0736-6

Koch, J., & Exner, C. (2015). Selective attention deficits in obsessive-compulsive disorder: The role of metacognitive processes. Psychiatry Research , 224 (3), 550–555.

Krakowski, A. D., et al. (2020). Inattention and hyperactive/impulsive component scores do not differentiate between Autism spectrum disorder and attention-deficit/hyperactivity disorder in a clinical sample. Mol Autism, 11 (1), 1–13.

Kushki, A., et al. (2019). Examining overlap and homogeneity in ASD, ADHD, and OCD: A Data-driven, diagnosis-agnostic approach. Translational Psychiatry . https://doi.org/10.1038/s41398-019-0631-2

Lang, R., et al. (2010). Influence of Assessment setting on the results of functional analyses of problem behavior. Journal of Applied Behavior Analysis, 43 (3), 565–567.

Article   MathSciNet   PubMed   PubMed Central   Google Scholar  

Luciana, M., et al. (2018). Adolescent neurocognitive development and impacts of substance use: Overview of the adolescent brain cognitive development (ABCD) baseline neurocognition battery. Developmental Cognitive Neuroscience, 32 , 67–79. https://doi.org/10.1016/j.dcn.2018.02.006

Article   CAS   PubMed   PubMed Central   Google Scholar  

Mick, E., Biederman, J., Pandina, G., & Faraone, S. V. (2003). A Preliminary Meta-Analysis of the Child Behavior Checklist in Pediatric Bipolar Disorder. Biological Psychiatry (pp. 1021–1027). Elsevier Inc.

Google Scholar  

Petty, C. R., et al. (2008). The child behavior checklist broad-band scales predict subsequent psychopathology: A 5-year follow-up. Journal of Anxiety Disorders, 22 (3), 532–539.

Piper, B. J., Gray, H. M., Raber, J., & Birkett, M. A. (2014). Reliability and validity of brief problem monitor, an abbreviated form of the child behavior checklist. Psychiatry and Clinical Neurosciences, 68 (10), 759–767.

Pollak, Y., Kahana-Vax, G., & Hoofien, D. (2008). Retrieval processes in adults with ADHD: A RAVLT study. Developmental Neuropsychology, 33 (1), 62–73.

Rey, A. 1964. “Rey Auditory Verbal Learning Test (AVLT).” The Clinical Examination in Psychology .

Rey, J. M., Schrader, E., & Morris-Yates, A. (1992). Parent-child agreement on children’s behaviours reported by the child behaviour checklist (CBCL). Journal of Adolescence, 15 (3), 219–230.

Shaw, M., et al. (2012). A systematic review and analysis of long-term outcomes in attention deficit hyperactivity disorder: effects of treatment and non-treatment. BMC Medicine . https://doi.org/10.1186/1741-7015-10-99

Toplak, M. E., West, R. F., & Stanovich, K. E. (2013). Practitioner review: Do performance-based measures and ratings of executive function assess the same construct? Journal of Child Psychology and Psychiatry, 54 (2), 131–143.

Tureck, K., et al. (2013). Investigation of the rates of comorbid symptoms in children with ADHD compared to children with ASD. Journal of Developmental and Physical Disabilities, 25 (4), 405–417.

Vakil, E., Blachstein, H., Wertman-Elad, R., & Greenstein, Y. (2012). Verbal learning and memory as measured by the rey-auditory verbal learning test: ADHD with and without learning disabilities. Child Neuropsychology, 18 (5), 449–466.

van Steensel, F. J. A., Bögels, S. M., & de Bruin, E. I. (2013). Psychiatric comorbidity in children with Autism spectrum disorders: A comparison with children with ADHD. Journal of Child and Family Studies, 22 (3), 368–376.

Weintraub, S., et al. (2013). Cognition assessment using the NIH toolbox. American Academy of Neurology, 80 (11 Suppl 3), S54–S64.

Williams, R. G., Klamen, D. A., & McGaghie, W. C. (2003). Cognitive, social and environmental sources of bias in clinical performance ratings. Teaching and Learning in Medicine, 15 (4), 270–292.

Download references

This study was supported by the Alberta Children’s Hospital Foundation and the Owerko Centre at the Alberta Children’s Hospital Research Institute.

Author information

Authors and affiliations.

Faculty of Graduate Studies, University of Calgary, Calgary, AB, Canada

Kelsey Harkness

Alberta Children’s Hospital Research Institute, Calgary, AB, Canada

Kelsey Harkness, Signe Bray, Deborah Dewey & Kara Murias

Hotchkiss Brain Institute, Calgary, AB, Canada

Alberta Health Services, Calgary, AB, Canada

Chelsea M. Durber

Cumming School of Medicine, University of Calgary, Calgary, AB, Canada

Signe Bray, Deborah Dewey & Kara Murias

You can also search for this author in PubMed   Google Scholar

Contributions

KH: Conceptualization, Methodology, Formal Analysis, Data Curation, Writing – Original Draft, Writing – Review & Editing, Visualization SB: Conceptualization, Methodology, Writing – Review & Editing, Supervision CMD: Writing – Review & Editing DD: Writing – Review & Editing KM: Conceptualization, Methodology, Resources, Writing – Review & Editing, Supervision.

Corresponding author

Correspondence to Kelsey Harkness .

Ethics declarations

Conflict of interest.

The authors have no example conflicts of interest to disclose.

Additional information

Publisher's note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Reprints and permissions

About this article

Harkness, K., Bray, S., Durber, C.M. et al. Assessing the Contribution of Measures of Attention and Executive Function to Diagnosis of ADHD or Autism. J Autism Dev Disord (2024). https://doi.org/10.1007/s10803-024-06275-9

Download citation

Accepted : 29 January 2024

Published : 13 March 2024

DOI : https://doi.org/10.1007/s10803-024-06275-9

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

  • Attention Deficit Hyperactivity Disorder (ADHD)
  • Executive Function (EF)
  • Find a journal
  • Publish with us
  • Track your research

Attention-Deficit/Hyperactivity Disorder Medications and Long-Term Risk of Cardiovascular Diseases

Affiliations.

  • 1 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
  • 2 Unit of Cardiology, Heart and Vascular Division, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
  • 3 School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
  • 4 Department of Applied Health Science, School of Public Health, Indiana University, Bloomington.
  • 5 Department of Psychological and Brain Sciences, Indiana University, Bloomington.
  • PMID: 37991787
  • PMCID: PMC10851097
  • DOI: 10.1001/jamapsychiatry.2023.4294

Importance: Use of attention-deficit/hyperactivity disorder (ADHD) medications has increased substantially over the past decades. However, the potential risk of cardiovascular disease (CVD) associated with long-term ADHD medication use remains unclear.

Objective: To assess the association between long-term use of ADHD medication and the risk of CVD.

Design, setting, and participants: This case-control study included individuals in Sweden aged 6 to 64 years who received an incident diagnosis of ADHD or ADHD medication dispensation between January 1, 2007, and December 31, 2020. Data on ADHD and CVD diagnoses and ADHD medication dispensation were obtained from the Swedish National Inpatient Register and the Swedish Prescribed Drug Register, respectively. Cases included individuals with ADHD and an incident CVD diagnosis (ischemic heart diseases, cerebrovascular diseases, hypertension, heart failure, arrhythmias, thromboembolic disease, arterial disease, and other forms of heart disease). Incidence density sampling was used to match cases with up to 5 controls without CVD based on age, sex, and calendar time. Cases and controls had the same duration of follow-up.

Exposure: Cumulative duration of ADHD medication use up to 14 years.

Main outcomes and measures: The primary outcome was incident CVD. The association between CVD and cumulative duration of ADHD medication use was measured using adjusted odds ratios (AORs) with 95% CIs.

Results: Of 278 027 individuals with ADHD aged 6 to 64 years, 10 388 with CVD were identified (median [IQR] age, 34.6 [20.0-45.7] years; 6154 males [59.2%]) and matched with 51 672 control participants without CVD (median [IQR] age, 34.6 [19.8-45.6] years; 30 601 males [59.2%]). Median (IQR) follow-up time in both groups was 4.1 (1.9-6.8) years. Longer cumulative duration of ADHD medication use was associated with an increased risk of CVD compared with nonuse (0 to ≤1 year: AOR, 0.99 [95% CI, 0.93-1.06]; 1 to ≤2 years: AOR, 1.09 [95% CI, 1.01-1.18]; 2 to ≤3 years: AOR, 1.15 [95% CI, 1.05-1.25]; 3 to ≤5 years: AOR, 1.27 [95% CI, 1.17-1.39]; and >5 years: AOR, 1.23 [95% CI, 1.12-1.36]). Longer cumulative ADHD medication use was associated with an increased risk of hypertension (eg, 3 to ≤5 years: AOR, 1.72 [95% CI, 1.51-1.97] and >5 years: AOR, 1.80 [95% CI, 1.55-2.08]) and arterial disease (eg, 3 to ≤5 years: AOR, 1.65 [95% CI, 1.11-2.45] and >5 years: AOR, 1.49 [95% CI, 0.96-2.32]). Across the 14-year follow-up, each 1-year increase of ADHD medication use was associated with a 4% increased risk of CVD (AOR, 1.04 [95% CI, 1.03-1.05]), with a larger increase in risk in the first 3 years of cumulative use (AOR, 1.08 [95% CI, 1.04-1.11]) and stable risk over the remaining follow-up. Similar patterns were observed in children and youth (aged <25 years) and adults (aged ≥25 years).

Conclusions and relevance: This case-control study found that long-term exposure to ADHD medications was associated with an increased risk of CVDs, especially hypertension and arterial disease. These findings highlight the importance of carefully weighing potential benefits and risks when making treatment decisions about long-term ADHD medication use. Clinicians should regularly and consistently monitor cardiovascular signs and symptoms throughout the course of treatment.

Publication types

  • Attention Deficit Disorder with Hyperactivity* / epidemiology
  • Cardiovascular Diseases* / epidemiology
  • Case-Control Studies
  • Hypertension*
  • Risk Assessment

Attention Deficit Hyperactivity Disorder in Children Essay

Diagnostic information (psychopathology).

The child’s patterns of inattention, physical agitation, lack of focus in studies, and restlessness attribute to the diagnosis of Attention Deficit Hyperactivity Disorder (ADHD). Indeed, the purposeless distractibility and reduced attention span of Jonathan attribute to the preliminary symptoms of ADHD as evidenced by the clinical literature (Millichap, 2010, p. 33). The behavioral treatment of ADHD focuses on strategically implementing positive reinforcement approaches following the DSM – IV standards. The criterion specified by DSM – IV-TR systematically categorizes ADHD into three stages including ADHD (Predominantly Inattentive), ADHD (Predominantly Hyperactive-Impulsive), and ADHD (Predominantly Combined) (Dziegielewski, 2014, p. 146). The child’s cognitive distortions including distraction and agitation require effective treatment with behavioral strategies advocating the depletion of emotional obstacles for reducing the distressing feelings and negative thoughts (Solanto, 2011, pp. 132-139). The provision of social rewards and encouraging remarks for initiating positive behavioral patterns in Jonathan will certainly enhance his focus and attention leading to emotional and behavioral stability. The intensive behavior therapy recommended by Brown (2009, p. 389) advocates the positive influence of training sessions, consultation programs, and summer treatment episodes and contingency management strategies resulting in positive clinical outcomes. Furthermore, the caretaker requires configuring reasonable and age-appropriate expectations from the child to facilitate its timely accomplishment with the implementation of behavioral strategies. The consistent utilization of effective praises and social rewards indeed results in the behavioral orientation of the child following the treatment goals.

Medical Treatment (Biopsychology/Psychopharmacology)

The research studies reveal the first-line therapy (including stimulant and non – stimulant drugs) for treating the episodes of ADHD among children and adolescents (Burns, Richardson & Brady, 2010, p. 182). The stimulant medications for treating ADHD include amphetamine and methylphenidate drugs; however, the non-stimulant drug atomoxetine is known for its pharmacological actions in reducing ADHD symptoms. Indeed, Vyvanse (lisdexamfetamine dimesylate) could suitably treat Jonathan’s symptoms of agitation, inattention, lack of focus, and distraction. The research studies reveal the effectiveness of Vyvanse in improving working and episodic memory, and cognitive control among the treated population. The initial dose of Vyvanse in treating ADHD is attributed to 30 mg/day among children within the age range of 6 – 12 years (Chew, Hales & Yudofsky, 2009, p. 353). Indeed, Vyvanse instigates task motivation and proportionately enhances performance among students while improving their stamina and reaction time through induction of dopamine reuptake inhibition across the central nervous system. This drug further instills confidence and concentration among the care seekers and therefore, is considered as the best therapeutic remedy for enhancing Jonathan’s performance in relation to his ADHD symptoms. Vyvanse induces efficacy for 12 hours daily and provides sustained effects in a couple of weeks with gradual dose increments accounting to the maximum of 70 mg on daily basis. The consistent administration of Vyvanse provides relief for an extended tenure; however, its growth-suppressive property does not encourage the physician to administer the medicine for a very long tenure. Therefore, this therapy is indeed not suitable for providing permanent treatment to the target population.

Therapy (Learning/Psychopathology/Intelligence/Cognition/Motivation/Emotion)

The treatment best suited for mitigating Jonathan’s symptoms of distraction, agitation follows the contention of the American Academy of Pediatrics advocating the blend of behavioral, and medication approaches for therapeutic intervention (Brock, Jimerson & Hansen, 2009, p. 135). In addition to the medication intervention, Jonathan requires consistent feedback from teachers and parents in the context of their performance-related expectations (from Jonathan). Furthermore, the short-term behavioral goals prove beneficial in improving Jonathan’s performance across family and school environments. The reward and recognition system following the behavioral modification would motivate Jonathan in accomplishing the clinical goals in the shortest possible interval. Indeed, the patterns of intelligence among children affected with ADHD do not exhibit any direct impact on the progression of the disease. The patients with increased intelligence levels continue experiencing inattention and distraction leading to underachievement, irrespective of their intelligence quotient (Kooij, 2013, p. 41). Indeed, Jonathan does not prove problematic for peers and family members and continues displaying curiosity and academic accomplishment during the initial months at school. Therefore, he does have the instincts and motivation for resuming normal behavior.

Family Support (Developmental Psychology, Personality, Health & Stress)

Brown (2009, p. 318) reveals the family history of substance abuse and other comorbidities among family members in established cases of ADHD. The disrupted relationships with parents and caretakers affected with substance abuse adversely affect the behavior of children affected with ADHD. Ryan and McDougall (2009, p. 81) reveal the patterns of behavioral disorientation among children affected by disorganized attachments with their family members. Indeed, the support extended by the patient’s family members through effective counseling and coping strategies potentially assists the child affected with ADHD in overcoming behavioral instability. The expenses incurred in utilizing treatment therapy and psychological counseling indeed financially affect the patient and his family members. Furthermore, Jonathan’s family requires clinical assistance for understanding the patterns of ADHD and effective coping strategies in supporting him in mitigating the behavioral outcomes. The personality traits exhibited by Jonathan attribute to decreased willpower, predisposition to developing other psychological manifestations, decreased listening skills, and instincts related to overlooking the details, thereby resulting in performance errors. The patterns of stress indeed, add up to the clinical manifestations of Jonathan in an ADHD set.

The Psychological Challenges & Community Support

The research studies reveal the psychological challenges attributed to frustration and anger among ADHD patients that aggravate further under the influence of family and school environment (Plotnik & Kouyoumdjian, 2014, p. 31). Jonathan’s agitation increases under the work constraints imposed by his teacher in his school environment. The evidence-based academic literature reveals the assistance extended by CHADD (Children and Adults with Attention Deficit Disorders) to the patients of ADHD and their families in effective mitigation of the patterns of clinical manifestations (Rief, 2005). These social organizations extend support structures for ADHD patients while configuring long and short-term goals in treating the functional difficulties experienced in the community environment.

The cultural perspectives profoundly influence the patterns of ADHD among the affected children. The other multiple factors attributing to the development of ADHD include the conditions of infection, poor nutrition, substance abuse, toxicity, and hereditary and cultural factors in the community setting. The patients affected by ADHD may exhibit dangerous influences on themselves as well as the society; however, the treatment approaches are affected by the cultural, historical, and psychosocial outlook in the community environment. The best remedial strategies in treating ADHD among children include the blend of therapeutic and behavioral therapies and family counseling for mitigating the clinical outcomes. Indeed, the behavioral modification among ADHD patients induced with effective family training results in enhanced psychosocial outcomes. Furthermore, enhancement of social skills and cognitive abilities also influence the positive outcomes among ADHD patients in the community environment.

Brock, S.E., Jimerson, S.R., & Hansen, R.L. (2009). Identifying, Assessing, and Treating ADHD at School . New York: Springer.

Brown, T.E. (2009). ADHD Comorbidities: Handbook for ADHD Complications in Children and Adults . USA: American Psychiatric Publishing.

Burns, C., Richardson, B., & Brady, M. (2010). Pediatric Primary Care Case Studies . USA: Jones & Bartlett.

Chew, R.H., Hales, R.E., & Yudofsky, S.C. (2009). What Your Patients Need to Know about Psychiatric Medications (2 nd ed). USA: American Psychiatric Publishing.

Dziegielewski, S.F. (2014). DSM-IV-TR in Action: Includes DSM-5 Update Chapter (2 nd ed). New Jersey: Wiley.

Kooij, J.J.S. (2013). Adult ADHD: Diagnostic Assessment and Treatment . London: Springer – Verlag.

Millichap, J.G. (2010). Attention Deficit Hyperactivity Disorder Handbook: A Physician’s Guide to ADHD . New York: Springer.

Plotnik, R., & Kouyoumdjian, H. (2014). Introduction to Psychology . USA: Wadsworth – Cengage.

Rief, S.F. (2005). How To Reach And Teach Children with ADD / ADHD: Practical Techniques, Strategies, and Interventions (2 nd ed). USA: Jossey – Bass.

Ryan, N., & McDougall, T. (2009). Nursing Children and Young People with ADHD . New York: Routledge.

Solanto, M.V. (2011). Cognitive-Behavioral Therapy for Adult ADHD: Targeting Executive Dysfunction . New York: Guiltford.

  • Chicago (A-D)
  • Chicago (N-B)

IvyPanda. (2022, January 25). Attention Deficit Hyperactivity Disorder in Children. https://ivypanda.com/essays/attention-deficit-hyperactivity-disorder-in-children/

"Attention Deficit Hyperactivity Disorder in Children." IvyPanda , 25 Jan. 2022, ivypanda.com/essays/attention-deficit-hyperactivity-disorder-in-children/.

IvyPanda . (2022) 'Attention Deficit Hyperactivity Disorder in Children'. 25 January.

IvyPanda . 2022. "Attention Deficit Hyperactivity Disorder in Children." January 25, 2022. https://ivypanda.com/essays/attention-deficit-hyperactivity-disorder-in-children/.

1. IvyPanda . "Attention Deficit Hyperactivity Disorder in Children." January 25, 2022. https://ivypanda.com/essays/attention-deficit-hyperactivity-disorder-in-children/.

Bibliography

IvyPanda . "Attention Deficit Hyperactivity Disorder in Children." January 25, 2022. https://ivypanda.com/essays/attention-deficit-hyperactivity-disorder-in-children/.

  • Vyvanse – ADD and ADHD Medicine Company Analysis
  • Is Attention Deficit Hyperactivity Disorder Real?
  • Attention Deficit Hyperactivity Disorder (ADHD) in a Child
  • Understanding Attention-Deficit/Hyperactivity Disorder
  • ADHD: Mental Disorder Based on Symptoms
  • Attention Deficit Hyperactivity Disorder (ADD / ADHD)
  • Attention Deficit Hyperactivity Disorder Causes
  • Attention Deficit Hyperactivity Disorder: Signs and Strategies
  • Working Memory in Attention Deficit and Hyperactivity Disorder (ADHD)
  • Identifying, Assessing and Treating Attention Deficit Hyperactivity Disorder
  • Teaching Children and Its Aspects and Characteristics
  • NAEYC Standards and the 10 Principles of Caregiving
  • The Coping Cat Program: Critical Analysis
  • “Classroom Management Strategies for Difficult Students” by O’Farrell
  • Child Behaviour Plan Design
  • Research article
  • Open access
  • Published: 04 March 2024

Common and distinct cortical thickness alterations in youth with autism spectrum disorder and attention-deficit/hyperactivity disorder

  • Wanfang You 1 , 2 , 3   na1 ,
  • Qian Li 1 , 2   na1 ,
  • Lizhou Chen 1 , 2   na1 ,
  • Ning He 4 ,
  • Yuanyuan Li 4 ,
  • Fenghua Long 1 , 2 ,
  • Yaxuan Wang 1 , 2 ,
  • Yufei Chen 1 , 2 ,
  • Robert K. McNamara 5 ,
  • John A. Sweeney 1 , 5 ,
  • Melissa P. DelBello 5 ,
  • Qiyong Gong 1 , 2 &
  • Fei Li   ORCID: orcid.org/0000-0002-4737-5710 1 , 2  

BMC Medicine volume  22 , Article number:  92 ( 2024 ) Cite this article

850 Accesses

1 Altmetric

Metrics details

Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are neurodevelopmental disorders with overlapping behavioral features and genetic etiology. While brain cortical thickness (CTh) alterations have been reported in ASD and ADHD separately, the degree to which ASD and ADHD are associated with common and distinct patterns of CTh changes is unclear.

We searched PubMed, Web of Science, Embase, and Science Direct from inception to 8 December 2023 and included studies of cortical thickness comparing youth (age less than 18) with ASD or ADHD with typically developing controls (TDC). We conducted a comparative meta-analysis of vertex-based studies to identify common and distinct CTh alterations in ASD and ADHD.

Twelve ASD datasets involving 458 individuals with ASD and 10 ADHD datasets involving 383 individuals with ADHD were included in the analysis. Compared to TDC, ASD showed increased CTh in bilateral superior frontal gyrus, left middle temporal gyrus, and right superior parietal lobule (SPL) and decreased CTh in right temporoparietal junction (TPJ). ADHD showed decreased CTh in bilateral precentral gyri, right postcentral gyrus, and right TPJ relative to TDC. Conjunction analysis showed both disorders shared reduced TPJ CTh located in default mode network (DMN). Comparative analyses indicated ASD had greater CTh in right SPL and TPJ located in dorsal attention network and thinner CTh in right TPJ located in ventral attention network than ADHD.

Conclusions

These results suggest shared thinner TPJ located in DMN is an overlapping neurobiological feature of ASD and ADHD. This alteration together with SPL alterations might be related to altered biological motion processing in ASD, while abnormalities in sensorimotor systems may contribute to behavioral control problems in ADHD. The disorder-specific thinner TPJ located in disparate attention networks provides novel insight into distinct symptoms of attentional deficits associated with the two neurodevelopmental disorders.

Trial registration

PROSPERO CRD42022370620. Registered on November 9, 2022.

Peer Review reports

Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are prevalent neurodevelopmental disorders in children and adolescents. ASD is characterized by social impairments, communication deficits, restricted interests, and stereotypical repetitive behaviors, while ADHD is defined by inattention, hyperactivity, and impulsivity [ 1 ]. Although different in many respects, it has been widely recognized that ASD and ADHD have overlapping behavioral features [ 2 , 3 ] and genetic liability [ 4 ]. Specifically, social impairment and attention deficits are implicated in both disorders [ 2 ], and there are shared difficulties in other cognitive and behavioral traits [ 3 ]. Exploring brain structure could help understand the neurobiological basis which builds the bridge between the shared and different clinical manifestations and genetic liability of the two disorders. Currently, the overlapping and distinct brain mechanisms contributing to these two disorders remain to be clarified.

Previous structural magnetic resonance imaging (MRI) studies have revealed brain alterations in both ASD and ADHD [ 5 , 6 , 7 , 8 ]. Relative to typically developing controls (TDC), studies of ASD have demonstrated multiple regional morphological changes, some of which have been associated with social and behavioral features of autism [ 6 ]. In one study, individuals with ASD showed gray matter concentration increases prominently in the frontal, parietal, and occipital lobes, as well as subcortical regions, and decreases were observed in the temporoparietal junction (TPJ) [ 9 ]. Several studies of ADHD indicate that this disorder as well may result from delayed brain maturation, with delayed maturation of cortical volume, thickness, and surface area in pediatric patients with ADHD compared to TDC [ 7 , 10 , 11 ]. More recently, neuroimaging studies have begun to directly compare patients with ASD, ADHD, and comorbid individuals, and the findings of such studies have been inconsistent [ 12 ]. For example, overlapping abnormalities of reduced gray matter volume (GMV) in the left temporal lobe were seen in both ASD and ADHD [ 13 ], while another study found that enlarged GMV in left temporal cortex only in ASD [ 14 ]. These and other inconsistencies may be due to small samples with clinical heterogeneities [ 13 , 14 ]. Therefore, a meta-analytic approach is well-suited to identify the most replicable overlapping and disorder-specific brain alterations in these disorders.

There have been previous meta-analytic efforts to compare alterations of brain anatomy in ASD and ADHD. A voxel-based meta-analysis of volumetric measurements reported increased bilateral temporal and right dorsolateral prefrontal volume in ASD and decreased ventromedial orbitofrontal volume for ADHD [ 15 ]. Another meta-analysis did not find significant differences in brain gyrification between the two disorders or between each disorder and TDC [ 16 ]. Cortical thickness (CTh) is a sensitive metric for evaluating cortical maturation abnormalities in clinical populations [ 17 , 18 ]. Of note, it is sensitive to alterations in the maturation in the columnar organization of the neocortical mantle. Also, as regional volume measurements reflect combined influences of cortical morphology, examining CTh separately may advance neurobiological understanding of neurodevelopmental disorders [ 19 ]. ENIGMA consortium has found subtle overlapping cortical thinning in precentral gyrus and temporal lobes between the two disorders in children [ 20 ]. This study recruited data from multi-consortium sites rather than summarizing the data from existing publications and analyzed the average CTh in 68 cortical regions defined by the Desikan–Killiany atlas. The whole-brain vertex-based analysis might better address the issue of atlas bias in findings and report between-group differences in a more accurate brain location.

Another important issue for previous meta-analyses is that they included individuals with wide-ranging age groups [ 15 , 16 , 21 ]. For example, patients aged from less than 10 to over 60 in one study [ 21 ]. This is a potential limitation as structural abnormalities vary at different ages in both ASD [ 6 ] and ADHD [ 7 ], with children and adolescents having more significant atypicality than adults [ 22 ]. For example, atypicality of frontal, occipital, and parietal cortical volumes has been shown to be greater in adolescents than in adults with ASD [ 22 ]. Therefore, exploring brain features in children and adolescents may be more sensitive to detect neurodevelopmental alterations in brain maturation in ASD and ADHD, and their similarities and differences.

For these reasons, we conducted a whole-brain vertex-based CTh meta-analysis, with CTh measured as the distance between the gray-white interface and the pia mater. A recently developed mask for surface-based meta-analysis was used, which has been used previously in studies of other neuropsychiatric disorders [ 23 ]. To identify shared and disorder-specific CTh abnormalities in ASD and ADHD, a quantitative, vertex-based meta-analytic comparison of published whole-brain structural MRI studies in children and adolescents with ASD and ADHD was performed.

Search strategy and study inclusion

The present study was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (see Additional file 1 : Table S1). A systematic search was conducted for peer-reviewed English language publications in PubMed, Web of Science, Embase, and Science Direct from inception to 8 December 2023. Keywords related to ASD (“autism” or “autistic” or “ASD” or “autism spectrum disorder”) and ADHD (“hyperkinetic” or “ADHD” or “attention-deficit/hyperactivity disorder”) plus terms associated with structural imaging (“cortical thickness” or “thickness”) were used for the literature search. A manual search was further conducted in the bibliographies of the retrieved studies and relevant reviews or meta-analyses.

The inclusion criteria for eligible studies included: (1) all participants were younger than 18 years of age and compared CTh between either of ASD and ADHD groups and TDC, (2) applied vertex-based or surface-based method, (3) estimated whole-brain CTh changes to remove bias inherent in regions-of-interest analysis, and (4) provided the peak coordinates of results in stereotactic space (Montreal Neurological Institute (MNI) or Talairach). We focused on the vertex-level whole-brain studies and excluded template-based studies even if the template covered the whole brain to reduce methodological heterogeneity and improve the spatial accuracy of results. Studies containing multiple independently analyzed subgroups were treated as separate datasets. For studies with multiple publications using overlapping samples, the one with the largest sample was included. Conference papers, case reports, and mega-analyses were excluded. Eligible studies reporting no between-group differences were included and estimated conservatively to have a null effect size. Studies were independently ascertained by two researchers (WFY and LZC) and checked by the corresponding author (FL). Any inconsistency was discussed under FL’s guidance until a consensus was reached. The protocol (registration number: CRD42022370620) was registered in the international prospective register of systematic reviews (PROSPERO).

Quality assessment

There were four ASD studies [ 24 , 25 , 26 , 27 ] and two ADHD studies [ 28 , 29 ] that could not be included due to unavailable coordinates of the cortical thickness (CTh) results after the corresponding authors were contacted for missing information (Additional file 1 : Table S2). We applied the 12-point checklist to assess methodology quality of the included studies (Additional file 1 : Table S3). In the 12-point checklist, each point was scored as 0, 0.5, or 1 if the criteria were unfulfilled, partially met, or fully met, respectively. All studies included in the present meta-analysis scored more than eight points. The checklist was not designed to critique the investigators or the work itself, but to provide an objective indication of the rigor of the individual studies. All studies using public databases were listed in Additional file 1 : Table S4.

Mean age, mean IQ, proportion of males, comorbidity, medication status, preprocessing method, statistical threshold, and key findings of each study were summarized (Table 1 ). Effect size and coordinates of peaks for regional differences were also extracted for meta-analysis. Two co-authors (WFY and LZC) independently conducted the data extraction and the corresponding author (FL) double-checked the information.

  • Meta-analysis

Meta-analysis was performed using seed-based d mapping (SDM) software (version 5.15), a meta-analytic tool that has been widely employed in neuroimaging research of various modalities. The procedures of the SDM method have been described in detail elsewhere [ 48 ] and its key aspects are described here. First, meta-analysis was separately conducted in ASD and ADHD groups to identify abnormal regional CTh changes relative to healthy individuals in each disorder. These peak coordinates of results reported in Talairach space were first converted to MNI space by SDM software. After that, the SDM software uses the peak coordinates and effect sizes of clusters showing significant differences between patients and controls, including null effect size findings, to create an effect-size signed map and its variance map for each study, represented as an anisotropic Gaussian kernel. Both positive and negative results (increased/decreased CTh in patients than TDC) were reconstructed in the same map to avoid any voxel erroneously appearing positive and negative simultaneously. Then random-effects analysis was performed to obtain the mean map across studies, weighted by sample size, the variance of each study, and estimated between-study heterogeneity. Considering the heterogeneities of clinical characteristics, subgroup analyses were performed based on medication status and comorbidity in each disorder using the same threshold as the pooled meta-analysis, when the subgroups included five or more datasets ( n  ≥ 5) as suggested [ 49 ].

A quantitative comparison of CTh was then performed between the two disorders, and standard randomization tests were used to establish statistical significance with mean age and proportion of males as covariances. The conjunction and disjunction analyses were performed to identify overlapping and divergent abnormalities across ASD and ADHD relative to TDC. A random-effects general linear meta-regression was conducted between significant CTh clusters and mean age, mean IQ, and proportion of male patients in each disorder. We also examined linear and nonlinear age-related changes in CTh, as there are non-linear patterns of age-related changes in CTh [ 50 ]. Full details of jackknife, heterogeneity and publication bias analysis, and meta-regression analysis are provided in Additional file 1 : Supplementary Methods.

All meta-analyses were conducted with the default SDM threshold ( P  < 0.005, Z  > 1.0 with cluster extent > 10 voxels), which has been found to optimally balance sensitivity and specificity and provide an approximate equivalent to corrected P value = 0.05 in SDM [ 48 ]. A more stringent probability threshold was employed for meta-regression ( P  < 0.0005) and conjunction and disjunction analyses ( P  < 0.0025) as suggested [ 48 ].

Study characteristics

Our search strategy yielded ten ASD studies [ 9 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 ] and nine ADHD studies [ 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 ] that met the abovementioned inclusion criteria (Fig. 1 ). Among them, two ASD studies [ 37 , 38 ] and one ADHD study [ 45 ] contained two independent patient sample sets. Of note, one ASD study examined both children and adults [ 41 ], and we only used the children subgroup dataset in our analyses.

figure 1

Flowchart of literature search and eligibility assessment

Therefore, a total of 12 ASD datasets involving 458 patients with ASD (age 10.2 ± 3.3 years, IQ 104.1 ± 5.8, males/females 413/45) and 472 controls (age 11.1 ± 2.7 years, IQ 109.8 ± 5.0, males/females 412/60), and 10 ADHD datasets involving 383 patients with ADHD (age 11.4 ± 1.5 years, IQ 103.7 ± 4.4, males/females 326/57) and 380 controls (age 11.5 ± 1.7, IQ 108.0 ± 1.9, males/females 292/88) were included. None of these studies had significant differences in age and sex between patients and controls. In the present study, youth in the two groups with ASD and ADHD had no significant statistical differences in age ( P  > 0.05). The proportion of males in the ASD group is slightly higher than that in the ADHD group ( χ 2  = 5.005, P  = 0.025). Eight datasets did not report if IQ was matched between groups [ 30 , 34 , 38 , 39 , 41 , 43 , 47 ], six datasets found significantly higher IQ in controls than patients [ 9 , 31 , 32 , 37 , 40 , 42 ], and there were no between-group differences in IQ in the remaining studies.

As for the medication and comorbidities, there was one ASD dataset recruiting patients who discontinued medications before MR scans [ 31 ], and the other ASD studies did not clarify treatment status of their participants. There were two ASD studies included pure ASD patients without any other psychiatric disorders [ 9 , 36 ], one ASD study reported comorbidities of ADHD and anxiety disorder [ 38 ], and the others did not report comorbidity or only excluded patients with neurological or genetic diseases, e.g., tuberous sclerosis and fragile X. In ADHD, there were six ADHD datasets that recruited medication-naïve patients [ 44 ] or patients who discontinued medications before MR scans [ 39 , 40 , 43 , 45 ]. Three ADHD datasets [ 41 , 42 , 46 ] used medicated patients and one dataset did not clearly indicate the medication status [ 47 ]. With regard to comorbidities, six ADHD datasets recruited pure ADHD patients [ 39 , 41 , 43 , 44 , 45 , 46 ] while four ADHD datasets reported that some patients had comorbid conduct disorder, oppositional defiant disorder [ 40 , 45 ], epilepsy [ 42 ], and behavioral and anxiety related disorder [ 47 ]. It should be noted that patients with a history of cannabis use [ 43 ] were not considered as a comorbidity in the current study.

Compared with TDC, patients with ASD showed increased CTh in bilateral superior frontal gyrus, left middle temporal gyrus, and right superior parietal lobule (SPL), and decreased CTh in right TPJ (Table 2 , Figs. 2 and 3 C , Additional file 1 : Fig. S1). Egger’s test of funnel plot asymmetry was not statistically significant in all brain regions (all P  > 0.05), failing to identify publication bias in ASD studies. None of the brain regions with altered CTh showed statistically significant heterogeneity between studies except for the increased CTh in left superior frontal gyrus ( Z  = 1.676, P  < 0.001). The jackknife sensitivity analysis found that all results were preserved in 11 combinations out of 12 datasets. The number of ASD studies was insufficient for subgroup analysis about medication and comorbidities.

figure 2

Cortical thickness alterations in ASD and ADHD. The SDM software uses the peak coordinates and effect sizes of clusters showing significant difference between patients and controls to create an effect-size signed map and its variance map for each study. Then random-effects analysis was performed to obtain the mean map of included studies, weighted by sample size, the variance of each study, and between-study heterogeneity. The boundary of the result clusters in the mean map was determined by corresponding statistical thresholds. Subsequently, the results maps of ASD vs controls, ADHD vs controls, and the comparison between ASD and ADHD were mapped onto the Colin 27 brain template to generate Fig. 2

figure 3

Illustration of CTh alterations in right TPJ in ASD and ADHD in present meta-analysis. The results maps of ASD group, ADHD group, and the comparison and conjunction between ASD and ADHD in right temporoparietal junction (TPJ) were mapped onto the Smoothed International Consortium for Brain Mapping 152 to generate Fig. 3. A shows the brain regions of ventral (yellow areas) and dorsal (blue areas) attention networks respectively on the right hemisphere based on Yeo 7 network template [ 51 ]. B delineates the conjunctively decreased CTh (orange areas) in right TPJ shared in both ASD and ADHD. C and D demonstrate decreased CTh in right TPJ in ASD (green areas) and ADHD (purple areas) than their respective typically developing controls. E and F present a more severe CTh decreases in right TPJ in ASD than ADHD (pink areas) and in ADHD than ASD (red areas)

It should be noted that most samples were school-age children and adolescents, except one ASD study analyzed a cohort of preschool-aged children of 2 to 5 years old [ 30 ]. In jackknife sensitivity analysis, we excluded the dataset [ 30 ] using preschool children. After that, the thickness of left superior frontal gyrus was not significantly increased in ASD compared with TDC. However, in other combinations for sensitivity analysis, the brain regions with increased CTh and their locations remained exactly the same as in the pooled meta-analysis of ASD studies. In linear and nonlinear meta-regression with pooled studies, ASD studies with younger patients related to thicker CTh in left superior frontal gyrus (both regression P  < 0.0005). After removing the preschool children study [ 30 ], the age trend of this brain region was no longer significant, which means the regression result with pooled studies was unstable. No similar relationship was found between CTh and male percentage or mean IQ in this region. Therefore, the increased CTh in left superior frontal gyrus having heterogeneity might come from the influence of the inclusion of preschool children.

Compared with TDC, patients with ADHD showed decreased CTh in right precentral gyrus (extending to right postcentral gyrus), left precentral gyrus, and right TPJ (Table 2 , Figs. 2 and 3 D, Additional file 1 : Fig. S2). There was no evidence of publication bias in any cluster. None of the regions with altered CTh showed significant heterogeneity between studies. The jackknife analysis found that decreased CTh in bilateral precentral gyri was preserved in 8 combinations out of 10 datasets. Decreased CTh in the right TPJ remained significant in 9 combinations of ADHD studies. Consistent with the pooled results, the subgroup analysis of patients without comorbidity revealed decreased CTh in right precentral gyrus (extending to right postcentral gyrus), superior frontal gyrus, left precentral gyrus, cingulated gyrus, and bilateral TPJ compared to corresponding TDC (Additional file 1 : Table S5). The subgroup analysis of medication-free patients (including medication-naïve patients) revealed no differences in CTh between ADHD and TDC. Linear and nonlinear models of age effects, and effects of mean IQ and percentage of male patients, were all not significantly associated with abnormal CTh in ADHD.

Paralleling the above findings, conjunction analyses revealed a consistent CTh reduction in right TPJ in both ASD and ADHD compared with TDC (Table 2 , Figs. 2 and 3 B). To follow up this finding, we examined the effects in the different functional subareas of TPJ based on the Yeo 7 network template [ 51 ]. From anterior to posterior generally, subareas of TPJ belong to ventral attention network (VAN), default mode network (DMN), and dorsal attention network (DAN) (Fig. 3 A). In ASD, CTh was decreased in the right TPJ affiliated with the VAN and DMN, while ADHD CTh reductions in right TPJ were affiliated with the DAN and DMN.

Quantitative comparison between the two disorders revealed that participants with ASD demonstrated thinner CTh in right TPJ in subregions affiliated with the VAN (Fig. 3 E) and thicker CTh in right TPJ in subregions affiliated with the DAN and right SPL compared with ADHD (Table 2 , Figs. 2 and 3 F). No brain regions showed significant disjunctive CTh changes in ASD and ADHD. Furthermore, since there was heterogeneity in the meta-analysis of ASD studies, we discarded the study with preschool children and repeated the comparison of ASD and ADHD to test replicability and reliability of the results. Individuals with ASD also demonstrated more pronounced reductions of CTh in right TPJ in subregions affiliated with the VAN ( P  < 0.001, cluster size = 1337 voxels).

The present meta-analysis identified decreased CTh in a DMN-related subarea of right TPJ that was shared in ASD and ADHD. Effects in other regions differed between the disorders. Direct comparisons of the two disorders revealed that the ASD samples demonstrated increased CTh in right SPL and decreased CTh in the VAN subarea of right TPJ, while the ADHD samples showed reduced CTh in the DAN subarea of right TPJ. These results demonstrate that these two neurodevelopmental disorders have overlapping decreases in CTh in the DMN-affiliated subarea of right TPJ and distinct patterns of CTh abnormalities which represent a basis for understanding the greater problems of perception and social cognition in ASD and the greater behavioral control problems in ADHD. The general pattern of increases in CTh in ASD and decreases of CTh in ADHD also differentiated the disorders.

Common and distinct features of CTh reduction of right TPJ in ASD and ADHD

The right TPJ is a higher-order area of association cortex including the unimodal visual area V5 responsible for motion processing. TPJ subregions are functionally and anatomically connected with different brain networks [ 52 ]. The TPJ region is known to play key roles in integrating polysensory information, biological and general visual motion processing, and it is robustly modulated by top-down attentional control [ 52 ]. The activity of right TPJ in DMN has been linked to performance of theory of mind (ToM) tasks [ 53 ] and coactivation of medial prefrontal cortex and TPJ in DMN is increased during social cognition [ 54 ]. Our findings in TPJ are consistent with the problems of social cognition in both ASD and ADHD [ 55 , 56 ]. Delayed brain development in right TPJ has been described in both disorders as well, and they have been associated with abnormalities of mentalizing and social abilities in these neurodevelopmental disorders [ 57 , 58 ]. Thus, the dysmaturation of the TPJ region may be a robust transdiagnostic neuroimaging phenotypic biomarker relevant to the behavioral manifestation of both disorders, albeit in somewhat different ways given the subregions affected.

Impairments of right TPJ in ASD and ADHD have been reported using other neuroimaging modalities. The fractional anisotropy values of white matter between right TPJ and left frontal lobe were reduced in individuals with high-functioning autism and associated with decreased social emotionality [ 59 ]. TPJ alterations in ASD have been identified in a magnetoencephalography study which observed impaired connectivity between TPJ and frontal and temporal brain regions during a false-belief task (that is dependent on mentalizing and visual processing) in adults with ASD [ 60 ]. Functional MRI (fMRI) studies have identified atypical TPJ responses during visual motion processing [ 61 ]. Similarly, in adolescents with ADHD, impaired social cognition and communication have been related to altered functional connectivity between TPJ and precuneus [ 62 ].

However, while the TPJ was altered in both disorders, subregion analysis revealed a shared impact of the area associated with the DMN. ASD and ADHD exhibited different alterations in other TPJ subregions that are known to be affiliated with different attention networks [ 63 ]. Specifically, in ASD, a separate TPJ region with decreased CTh linked to the VAN was observed, while the additional TPJ reduction in ADHD was located in DAN. This difference implicates different attention network impairments in these two disorders. The VAN mediates the bottom-up attentional processing of novel external stimuli and is involved in detecting and reorienting attention to unexpected stimuli [ 64 ]. In contrast, DAN mediates top-down attentional processing involving internal guidance of attention based on prior knowledge, willful plans, and current goals [ 65 ]. These anatomic alterations are consistent with psychological studies demonstrating impaired attentional orienting to external stimulation in ASD [ 66 ] and difficulties in guiding voluntary allocation of attention in ADHD [ 67 ].

Increased CTh in ASD

Our study found that patients with ASD showed increased CTh in bilateral superior frontal gyrus, left middle temporal gyrus, and right SPL compared with TDC. This suggests a pattern of brain overgrowth or reduced age-related neuronal pruning, in widespread areas of association cortex. Widespread functional alterations of association cortex in ASD have also been reported, though their relation to increases of CTh remains to be fully examined [ 68 , 69 ]. The longitudinal study has clarified age-related abnormal trajectories of frontal, temporal, and superior parietal CTh in ASD, supporting models of both accelerated thickening and decelerated thinning particularly in early childhood resulting in increased CTh in later life in ASD [ 6 ]. Consistent with the neurodevelopmental interpretation of these findings, a neuroanatomical abnormality of a wide range of brain regions has been associated with polygenic risk for ASD [ 70 ]. Histological research has indicated that increased CTh in ASD could reflect an excess number of neurons [ 71 ] due to reduced synaptic pruning [ 72 ]. This neurodevelopmental mechanism might explain the increased CTh observed in the present study and the functional changes of neocortex in older children and adolescents with ASD [ 15 ].

Superior frontal abnormalities have been theorized to underlie socialization and cognitive control deficits in ASD [ 73 , 74 , 75 ]. Highlighting the divergences between regional increases of the cortical mantle in ASD and decreases in ADHD, the ENIGMA mega-analysis and other studies reported thicker frontal regions were specific to ASD relative to ADHD [ 73 ], an effect that has been related to the severity of the autism phenotype [ 74 , 75 ]. The comparative fMRI meta-analyses of cognitive control between ASD and ADHD have found specific underactivated dorsomedial prefrontal gyrus in ASD [ 15 ].

The larger GMV in the left middle temporal gyrus has also been correlated with social and communication deficits [ 76 ]. Our findings of increased left middle temporal CTh could partly explain the increased GMV of middle temporal gyrus in ASD observed in previous meta-analyses [ 77 ]. The left middle temporal gyrus is involved in language processing. The failure to develop normal language is one of the most common core features of ASD and is correlated with social and communication deficits.

The increase in SPL CTh was specific to ASD. As a region belonging to DAN, this region subserves visual attention and perceptual processes [ 78 ]. Taken together with the aberrant CTh in TPJ, its disturbance could account for dysfunctional top-down control of visuospatial attention in ASD [ 61 , 79 ]. Dysfunctional top-down control of visuospatial attention has been shown to be related to more severe repetitive behavior and restricted interest symptoms [ 80 , 81 ], and abnormal SPL structural and functional connectivity was one of the most informative features contributing to ASD classification and prediction models [ 82 ].

Decreased CTh in ADHD

In our study, participants with ADHD exhibited reduced CTh in bilateral motor cortices compared with TDC, an effect not observed in ASD. A multicenter research also approved that increased CTh in patients with ASD and thinner cortex in ADHD [ 21 ]. Longitudinal studies have shown that the ordered sequence of regional brain development in ADHD is similar to that seen in TDC, but the development was delayed [ 7 , 83 ]. This is consistent with the clinical observation that many individuals have a reduction in ADHD symptoms by early adulthood, by which time delayed maturation of brain systems may be complete [ 84 ]. Similar neurodevelopmental delay has been found in unaffected siblings of children with ADHD, suggesting a hereditary contribution to delayed brain maturation in ADHD [ 85 ].

Motor cortices use sensory information to generate adaptive behavioral plans [ 86 ] and have been linked to hyperactivity and impulsivity in ADHD [ 87 , 88 ]. Motor planning, both in its precision and implementation, is altered in ADHD and can contribute to developmental delay of higher-order motor control and impulsivity in ADHD. Correlations between abnormalities in motor cortices and worse performance in motor and response control tasks have been reported previously [ 89 ]. The cortical inhibition deficits linked to an alteration in the GABA (γ-aminobutyric acid)-ergic activity in motor cortices in children with ADHD has been reported as a potential mechanism for the observed anatomic alterations in precentral gyrus [ 90 ]. Decreased cortical thickness may be able to be alleviated following treatment with psychostimulants, suggesting that ongoing neurochemical and neurophysiological alterations may contribute to this abnormality in ADHD [ 91 ].

Clinical and methodological considerations

Previous GMV meta-analyses reported increased frontal lobe volume and decreased volume in temporal lobe and TPJ in individuals with ASD [ 77 ] and widespread decreases in GMV with no regions of increases in individuals with ADHD [ 15 , 92 ]. Because GMV is more closely associated with cortical surface area, and CTh is relatively stable and distinct from GMV heritably, the current CTh analysis represents an important extension of prior GMV meta-analyses. In the current CTh study, similar patterns of cortical differences between the two neurodevelopmental disorders were also observed. For example, the observed reduction in thickness of the left precentral gyrus in ADHD might partially account for the previously reported volume reduction in the corresponding region [ 15 ]. However, previous GMV meta-analyses, which employed young adults, did not reveal overlapping effects in the two disorders, which might be due to the differences in sample age [ 15 , 77 , 92 ]. Indeed, prior research indicated overlap in cortical abnormalities compared to controls existed in children with ASD and ADHD, but not in adult patients [ 73 ]. Together, these findings highlight the need for future prospective longitudinal studies employing different cortical metrics to provide a more comprehensive understanding of structural alterations over the course of neurodevelopment.

In addition to identifying differential neurobiological features in ASD and ADHD, the observed altered CTh patterns may have diagnostic implications [ 93 , 94 ]. For example, with machine learning applications, brain regions related to social and language were considered to be core features in identifying ASD, whereas regions related to motion are core features of ADHD [ 93 , 95 ]. Additionally, GMV in TPJ was found to classify good and poor responders to methylphenidate treatment in ADHD [ 96 ]. We speculate that integrating specific deficits in attention networks associated with TPJ observed in the present study may also be used to increase diagnostic accuracy and improve treatment outcomes in these disorders and warrants further exploration.

It should be noted that in this study, we were unable to exclude the possibility that the effects observed in patients were influenced by sex bias. In typically developing populations, sex has significant influences on the development of several brain regions, including prefrontal cortex and TPJ [ 97 ]. For example, females have thicker CTh in TPJ than age-matched males from late childhood and consistently through old ages [ 98 , 99 ]. It is common to include more males in ASD and ADHD studies due to the higher prevalence of both disorders in males. Sex has been demonstrated to impact the neuroanatomical alterations in ASD [ 100 ] and ADHD [ 29 ] both in effect extent and location and shape brain morphology during development. For example, males with ASD were characterized by cortical thickening while females exhibit cortical thinning [ 101 ]. Males with ASD have more significant temporal lobe gray matter enlargement compared with females [ 102 ], suggesting ASD males have more severe social and communication defects [ 100 ]. In ADHD, males have poorer motor performance than females which is related to a smaller premotor surface area in males [ 103 ]. However, the study design of the included original studies precluded us from performing subgroup analyses in male and female patients respectively. Larger respective studies of males and females are needed to better explore the potential impact of sex on the CTh alterations observed in these conditions [ 104 ].

Although ASD and ADHD are dynamic disorders with complex cortical changes over time from childhood into adulthood [ 7 , 50 , 70 ], we did not observe a significant association between age and altered CTh in the meta-regression analysis. This might be because only average age in study samples was extracted from each study for these analyses, which has limited the ability to precisely characterize age effects on brain CTh in ASD and ADHD. Nevertheless, we acknowledge that age is a crucial factor for brain developmental trajectories in neurodevelopmental disorders, and the greater heterogeneity found in preschool children in our analysis supports age-related effects.

Regarding methodological consideration, eligible studies included in our meta-analysis used two mainstream preprocessing methods, Freesurfer and CIVET. The geometrical accuracy of surface extraction is critical for the accurate measurement of CTh which could result in undetectable potential method heterogeneity. A comparative study found that CIVET reconstructs the most accurate surfaces and Freesurfer offers more realistic surfaces [ 105 ]. While potential differences exist between the two methods, they both demonstrate good geometric estimation of cortical surfaces. Similarly, the reconstruction of cortices was influenced by field strength and sequence parameters, especially the repetition time, which warrants consideration. These factors might subtly affect the contrast between gray and white matter and the extraction of white matter surface and the pial surfaces. While considered and evaluated statistically (i.e., significant heterogeneity in ASD), these methodological differences across studies represent an important consideration when interpreting our findings.

This meta-analysis has other limitations. First, the representativeness of the meta-analysis may be limited by the fact that many studies recruited high-functioning ASD individuals in neuroimaging research to promote successful MRI studies. This limits the ability to generalize the reported neuroimaging results to ASD with more severe behavioral and intellectual disabilities. Second, the effects of medication exposure cannot be explored by meta-regression and subgroup analysis in ASD groups because all studies did not report precise type and dose of medication, and only one study in ASD reported medicated status. Although we examined medication and comorbidity effects in ADHD studies, the statistical power was limited by the number of studies. Differences in psychotropic medication exposure between ASD and ADHD groups may have contributed to the differences between the two disorders. Third, although we did not find statistical differences in mean age between ASD and ADHD, the conjunctive results should be treated conservatively when considering the subtle mean age difference between ASD and ADHD groups. Fourth, the results of the original studies were reported in the standard space of the mature brain, and the use of a mask specifically created for children and adolescents would more accurately estimate spatial changes in the developing brain. Fifth, the current disorder-compared results are preliminary and indirect due to the scarcity of original studies comparing the two disorders in the same study. While our exploration could guide the design and further investigations of transdiagnostic studies. Last, more neuroimaging studies linking structural and functional alterations by using multimodal brain MRI methods [ 106 , 107 , 108 , 109 , 110 , 111 ] to better understand the functional effects of observed anatomic alterations are needed.

The case–control meta-analyses of ASD and ADHD found shared decreases in CTh in a subarea of right TPJ affiliated with the DMN. Other subregions of the TPJ were differentially affected in ASD and ADHD, which may explain divergent disturbances of attention in the two disorders. Other neocortical alterations in ADHD involved a thinning of CTh in motor cortices, while alterations of ASD involved increases of CTh in association cortices, highlighting a dramatic differentiation of neuroanatomic alterations in these two neurodevelopmental disorders. Our findings contribute to the understanding of differential and overlapping alterations of brain maturation in ASD and ADHD, which is important for the elucidation of disorder-specific etiologies.

Availability of data and materials

This study generated and analyzed the summary statistics of previous published studies. All data are available in these included articles. The statistical data of meta-analysis that support the findings of this study are available from the corresponding authors upon reasonable request.

Abbreviations

  • Attention-deficit/hyperactivity disorder
  • Autism spectrum disorder
  • Cortical thickness

Dorsal attention network

Default mode network

Functional MRI

Gray matter volume

Montreal Neurological Institute

  • Magnetic resonance imaging

Preferred Reporting Items for Systematic Reviews and Meta-Analyses

Prospective register of systematic reviews

Seed-based d mapping

Superior parietal lobule

Typically developing controls

Temporoparietal junction

Ventral attention network

Association AP. Diagnostic and statistical manual of mental disorders: DSM-5. 5th ed. Washington, D.C.: American Psychiatric Association; 2013.

Book   Google Scholar  

Krakowski AD, Cost KT, Anagnostou E, Lai MC, Crosbie J, Schachar R, et al. Inattention and hyperactive/impulsive component scores do not differentiate between autism spectrum disorder and attention-deficit/hyperactivity disorder in a clinical sample. Mol Autism. 2020;11(1):28.

Article   PubMed   PubMed Central   Google Scholar  

van der Meer JMJ, Lappenschaar MGA, Hartman CA, Greven CU, Buitelaar JK, Rommelse NNJ. Homogeneous combinations of ASD-ADHD traits and their cognitive and behavioral correlates in a population-based sample. J Atten Disord. 2017;21(9):753–63.

Article   PubMed   Google Scholar  

Ghirardi L, Brikell I, Kuja-Halkola R, Freitag CM, Franke B, Asherson P, et al. The familial co-aggregation of ASD and ADHD: a register-based cohort study. Mol Psychiatry. 2018;23(2):257–62.

Article   CAS   PubMed   Google Scholar  

Luo L, You W, DelBello MP, Gong Q, Li F. Recent advances in psychoradiology. Phys Med Biol. 2022;67(23):23TR01.

Zielinski BA, Prigge MB, Nielsen JA, Froehlich AL, Abildskov TJ, Anderson JS, et al. Longitudinal changes in cortical thickness in autism and typical development. Brain. 2014;137(Pt 6):1799–812.

Shaw P, Eckstrand K, Sharp W, Blumenthal J, Lerch JP, Greenstein D, et al. Attention-deficit/hyperactivity disorder is characterized by a delay in cortical maturation. Proc Natl Acad Sci USA. 2007;104(49):19649–54.

Article   ADS   CAS   PubMed   PubMed Central   Google Scholar  

Bu X, Gao Y, Liang K, Chen Y, Guo L, Huang X. Investigation of white matter functional networks underlying different behavioral profiles in attention-deficit/hyperactivity disorder. Psychoradiology. 2022;2(3):69–77.

Article   Google Scholar  

Foster NE, Doyle-Thomas KA, Tryfon A, Ouimet T, Anagnostou E, Evans AC, et al. Structural gray matter differences during childhood development in autism spectrum disorder: a multimetric approach. Pediatr Neurol. 2015;53(4):350–9.

Castellanos FX, Lee PP, Sharp W, Jeffries NO, Greenstein DK, Clasen LS, et al. Developmental trajectories of brain volume abnormalities in children and adolescents with attention-deficit/hyperactivity disorder. JAMA. 2002;288(14):1740–8.

Li F, Sun H, Biswal BB, Sweeney JA, Gong Q. Artificial intelligence applications in psychoradiology. Psychoradiology. 2021;1(2):94–107.

Rommelse N, Buitelaar JK, Hartman CA. Structural brain imaging correlates of ASD and ADHD across the lifespan: a hypothesis-generating review on developmental ASD-ADHD subtypes. J Neural Transmission (Vienna, Austria: 1996). 2017;124(2):259–71.

Brieber S, Neufang S, Bruning N, Kamp-Becker I, Remschmidt H, Herpertz-Dahlmann B, et al. Structural brain abnormalities in adolescents with autism spectrum disorder and patients with attention deficit/hyperactivity disorder. J Child Psychol Psychiatry. 2007;48(12):1251–8.

Lim L, Chantiluke K, Cubillo AI, Smith AB, Simmons A, Mehta MA, et al. Disorder-specific grey matter deficits in attention deficit hyperactivity disorder relative to autism spectrum disorder. Psychol Med. 2015;45(5):965–76.

Lukito S, Norman L, Carlisi C, Radua J, Hart H, Simonoff E, et al. Comparative meta-analyses of brain structural and functional abnormalities during cognitive control in attention-deficit/hyperactivity disorder and autism spectrum disorder. Psychol Med. 2020;50(6):894–919.

Gharehgazlou A, Freitas C, Ameis SH, Taylor MJ, Lerch JP, Radua J, et al. Cortical gyrification morphology in individuals with ASD and ADHD across the lifespan: a systematic review and meta-analysis. Cereb Cortex. 2021;31(5):2653–69.

Google Scholar  

Salat DH, Buckner RL, Snyder AZ, Greve DN, Desikan RS, Busa E, et al. Thinning of the cerebral cortex in aging. Cereb Cortex. 2004;14(7):721–30.

Shaw P, Kabani NJ, Lerch JP, Eckstrand K, Lenroot R, Gogtay N, et al. Neurodevelopmental trajectories of the human cerebral cortex. J Neurosci. 2008;28(14):3586–94.

Article   CAS   PubMed   PubMed Central   Google Scholar  

Winkler AM, Kochunov P, Blangero J, Almasy L, Zilles K, Fox PT, et al. Cortical thickness or grey matter volume? The importance of selecting the phenotype for imaging genetics studies. Neuroimage. 2010;53(3):1135–46.

Hoogman M, van Rooij D, Klein M, Boedhoe P, Ilioska I, Li T, et al. Consortium neuroscience of attention deficit/hyperactivity disorder and autism spectrum disorder: the ENIGMA adventure. Hum Brain Mapp. 2022;43(1):37–55.

Park MTM, Raznahan A, Shaw P, Gogtay N, Lerch JP, Chakravarty MM. Neuroanatomical phenotypes in mental illness: identifying convergent and divergent cortical phenotypes across autism, ADHD and schizophrenia. J Psych Neurosci. 2018;43(3):201–12.

Pretzsch CM, Schäfer T, Lombardo MV, Warrier V, Mann C, Bletsch A, et al. Neurobiological correlates of change in adaptive behavior in autism. Am J Psychiatry. 2022;179(5):336–49.

Li Q, Zhao Y, Chen Z, Long J, Dai J, Huang X, et al. Meta-analysis of cortical thickness abnormalities in medication-free patients with major depressive disorder. Neuropsychopharmacol. 2020;45(4):703–12.

Sharda M, Foster NEV, Tryfon A, Doyle-Thomas KAR, Ouimet T, Anagnostou E, et al. Language ability predicts cortical structure and covariance in boys with autism spectrum disorder. Cereb Cortex. 2017;27(3):1849–62.

Pappaianni E, Siugzdaite R, Vettori S, Venuti P, Job R, Grecucci A. Three shades of grey: detecting brain abnormalities in children with autism using source-, voxel- and surface-based morphometry. Eur J Neurosci. 2018;47(6):690–700.

Chen J, Wei Z, Liang C, Liu B, Guo J, Kong X, et al. Dysfunction of the auditory brainstem as a neurophysiology subtype of autism spectrum disorder. Front Neurosci. 2021;15:637079.

Li D, Liu C, Huang Z, Li H, Xu Q, Zhou B, et al. Common and distinct disruptions of cortical surface morphology between autism spectrum disorder children with and without SHANK3 deficiency. Front Neurosci. 2021;15:751364.

Narr KL, Woods RP, Lin J, Kim J, Phillips OR, Del’Homme M, et al. Widespread cortical thinning is a robust anatomical marker for attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2009;48(10):1014–22.

Almeida Montes LG, Prado Alcántara H, Martínez García RB, De La Torre LB, Avila Acosta D, Duarte MG. Brain cortical thickness in ADHD: age, sex, and clinical correlations. J Atten Disord. 2013;17(8):641–54.

Raznahan A, Lenroot R, Thurm A, Gozzi M, Hanley A, Spence SJ, et al. Mapping cortical anatomy in preschool aged children with autism using surface-based morphometry. NeuroImage Clin. 2012;2:111–9.

Duerden EG, Card D, Roberts SW, Mak-Fan KM, Chakravarty MM, Lerch JP, et al. Self-injurious behaviours are associated with alterations in the somatosensory system in children with autism spectrum disorder. Brain Struct Funct. 2014;219(4):1251–61.

Schaer M, Ottet MC, Scariati E, Dukes D, Franchini M, Eliez S, et al. Decreased frontal gyrification correlates with altered connectivity in children with autism. Front Hum Neurosci. 2013;7:750.

Dierker DL, Feczko E, Pruett JR Jr, Petersen SE, Schlaggar BL, Constantino JN, et al. Analysis of cortical shape in children with simplex autism. Cereb Cortex. 2015;25(4):1042–51.

Sussman D, Leung RC, Vogan VM, Lee W, Trelle S, Lin S, et al. The autism puzzle: diffuse but not pervasive neuroanatomical abnormalities in children with ASD. NeuroImage Clin. 2015;8:170–9.

Yang DYJ, Beam D, Pelphrey KA, Abdullahi S, Jou RJ. Cortical morphological markers in children with autism: a structural magnetic resonance imaging study of thickness, area, volume, and gyrification. Mol Autism. 2016;7(76):11.

Tanigawa J, Kagitani-Shimono K, Matsuzaki J, Ogawa R, Hanaie R, Yamamoto T, et al. Atypical auditory language processing in adolescents with autism spectrum disorder. Clin Neurophysiol. 2018;129(9):2029–37.

Kohli JS, Kinnear MK, Fong CH, Fishman I, Carper RA, Muller R-A. Local cortical gyrification is increased in children with autism spectrum disorders, but decreases rapidly in adolescents. Cerebral Cortex. 2019;29(6):2412–23.

Yin S, Hong SJ, Di Martino A, Milham MP, Park BY, Benkarim O, et al. Shared and distinct patterns of atypical cortical morphometry in children with autism and anxiety. Cereb Cortex. 2022;32(20):4565–75.

Qiu MG, Ye Z, Li QY, Liu GJ, Xie B, Wang J. Changes of brain structure and function in ADHD children. Brain Topogr. 2011;24(3–4):243–52.

de Zeeuw P, Schnack HG, van Belle J, Weusten J, van Dijk S, Langen M, et al. Differential brain development with low and high IQ in attention-deficit/hyperactivity disorder. PLoS ONE. 2012;7(4):e35770.

Article   ADS   PubMed   PubMed Central   Google Scholar  

Hoekzema E, Carmona S, Ramos-Quiroga JA, Richarte Fernández V, Picado M, Bosch R, et al. Laminar thickness alterations in the fronto-parietal cortical mantle of patients with attention-deficit/hyperactivity disorder. PLoS ONE. 2012;7(12):e48286.

Saute R, Dabbs K, Jones JE, Jackson DC, Seidenberg M, Hermann BP. Brain morphology in children with epilepsy and ADHD. PLoS ONE. 2014;9(4):e95269.

Çolak Ç, Çelik Z, Zorlu N, Kitiı Ö, Yüncü Z. Cortical thickness and subcortical volumes in adolescent synthetic cannabinoid users with or without ADHD: a preliminary study. Noro psikiyatri arsivi. 2019;56(3):167–72.

PubMed   PubMed Central   Google Scholar  

Lu L, Zhang L, Tang S, Bu X, Chen Y, Hu X, et al. Characterization of cortical and subcortical abnormalities in drug-naive boys with attention-deficit/hyperactivity disorder. J Affect Disord. 2019;250:397–403.

Vetter NC, Backhausen LL, Buse J, Roessner V, Smolka MN. Altered brain morphology in boys with attention deficit hyperactivity disorder with and without comorbid conduct disorder/oppositional defiant disorder. Hum Brain Mapp. 2020;41(4):973–83.

Lee J, Son JW, Kim S, Kim JE, Chung S, Ghim HR, et al. Disrupted association between empathy and brain structure in attention-deficit/hyperactivity disorder. Soa--ch’ongsonyon chongsin uihak=J Child Adolescent Psych. 2021;32(4):129–36.

Sarabin E, Harkness K, Murias K. The relationship between cortical thickness and executive function measures in children with and without ADHD. J Attention Disord. 2023;27(11):1263–71.

Radua J, Borgwardt S, Crescini A, Mataix-Cols D, Meyer-Lindenberg A, McGuire PK, et al. Multimodal meta-analysis of structural and functional brain changes in first episode psychosis and the effects of antipsychotic medication. Neurosci Biobehav Rev. 2012;36(10):2325–33.

Jackson D, Turner R. Power analysis for random-effects meta-analysis. Res Synth Methods. 2017;8(3):290–302.

Bethlehem RAI, Seidlitz J, White SR, Vogel JW, Anderson KM, Adamson C, et al. Brain charts for the human lifespan. Nature. 2022;604(7906):525–33.

Yeo BT, Krienen FM, Sepulcre J, Sabuncu MR, Lashkari D, Hollinshead M, et al. The organization of the human cerebral cortex estimated by intrinsic functional connectivity. J Neurophysiol. 2011;106(3):1125–65.

Doricchi F. The functions of the temporal-parietal junction. Handb Clin Neurol. 2022;187:161–77.

Schurz M, Tholen MG, Perner J, Mars RB, Sallet J. Specifying the brain anatomy underlying temporo-parietal junction activations for theory of mind: a review using probabilistic atlases from different imaging modalities. Hum Brain Mapp. 2017;38(9):4788–805.

Van Overwalle F. Social cognition and the brain: a meta-analysis. Hum Brain Mapp. 2009;30(3):829–58.

Miranda-Casas A, Baixauli-Fortea I, Colomer-Diago C, Roselló-Miranda B. Autism and attention deficit hyperactivity disorder: similarities and differences in executive functioning and theory of mind. Rev Neurol. 2013;57(Suppl 1):S177–84.

PubMed   Google Scholar  

Mary A, Slama H, Mousty P, Massat I, Capiau T, Drabs V, et al. Executive and attentional contributions to Theory of Mind deficit in attention deficit/hyperactivity disorder (ADHD). Child Neuropsychol. 2016;22(3):345–65.

Makris N, Biederman J, Valera EM, Bush G, Kaiser J, Kennedy DN, et al. Cortical thinning of the attention and executive function networks in adults with attention-deficit/hyperactivity disorder. Cereb Cortex. 2007;17(6):1364–75.

Eddy CM. The junction between self and other? Temporo-parietal dysfunction in neuropsychiatry. Neuropsychologia. 2016;89:465–77.

Mueller S, Keeser D, Samson AC, Kirsch V, Blautzik J, Grothe M, et al. Convergent findings of altered functional and structural brain connectivity in individuals with high functioning autism: a multimodal MRI study. PLos One. 2013;8(6):e67329.

Yuk V, Anagnostou E, Taylor MJ. Altered connectivity during a false-belief task in adults with autism spectrum disorder. Biol Psych Cognit Neurosci Neuroimaging. 2020;5(9):901–12.

Takarae Y, Luna B, Minshew NJ, Sweeney JA. Visual motion processing and visual sensorimotor control in autism. J Int Neuropsychol Soc: JINS. 2014;20(1):113–22.

Chen MH, Chen YL, Bai YM, Huang KL, Wu HJ, Hsu JW, et al. Functional connectivity of specific brain networks related to social and communication dysfunction in adolescents with attention-deficit hyperactivity disorder. Psychiatry Res. 2020;284:112785.

Katsuki F, Constantinidis C. Bottom-up and top-down attention: different processes and overlapping neural systems. Neuroscientist. 2014;20(5):509–21.

Vossel S, Geng JJ, Fink GR. Dorsal and ventral attention systems: distinct neural circuits but collaborative roles. Neuroscientist. 2014;20(2):150–9.

Wilterson AI, Nastase SA, Bio BJ, Guterstam A, Graziano MSA. Attention, awareness, and the right temporoparietal junction. Proc National Acad Sci United States of America. 2021;118(25):e2026099118.

Fitzgerald J, Johnson K, Kehoe E, Bokde AL, Garavan H, Gallagher L, et al. Disrupted functional connectivity in dorsal and ventral attention networks during attention orienting in autism spectrum disorders. Autism Res. 2015;8(2):136–52.

Salehinejad MA, Ghayerin E, Nejati V, Yavari F, Nitsche MA. Domain-specific involvement of the right posterior parietal cortex in attention network and attentional control of ADHD: a randomized, cross-over, sham-controlled tDCS study. Neuroscience. 2020;444:149–59.

D’Cruz AM, Mosconi MW, Ragozzino ME, Cook EH, Sweeney JA. Alterations in the functional neural circuitry supporting flexible choice behavior in autism spectrum disorders. Transl Psychiatry. 2016;6(10):e916.

Takarae Y, Minshew NJ, Luna B, Sweeney JA. Atypical involvement of frontostriatal systems during sensorimotor control in autism. Psychiatry Res. 2007;156(2):117–27.

Ecker C, Pretzsch CM, Bletsch A, Mann C, Schaefer T, Ambrosino S, et al. Interindividual differences in cortical thickness and their genomic underpinnings in autism spectrum disorder. Am J Psychiatry. 2022;179(3):242–54.

Courchesne E, Mouton PR, Calhoun ME, Semendeferi K, Ahrens-Barbeau C, Hallet MJ, et al. Neuron number and size in prefrontal cortex of children with autism. JAMA. 2011;306(18):2001–10.

Faust TE, Gunner G, Schafer DP. Mechanisms governing activity-dependent synaptic pruning in the developing mammalian CNS. Nat Rev Neurosci. 2021;22(11):657–73.

Boedhoe PSW, van Rooij D, Hoogman M, Twisk JWR, Schmaal L, Abe Y, et al. Subcortical brain volume, regional cortical thickness, and cortical surface area across disorders: findings from the ENIGMA ADHD, ASD, and OCD Working Groups. Am J Psychiatry. 2020;177(9):834–43.

van Rooij D, Anagnostou E, Arango C, Auzias G, Behrmann M, Busatto GF, et al. Cortical and subcortical brain morphometry differences between patients with autism spectrum disorder and healthy individuals across the lifespan: results from the ENIGMA ASD Working Group. Am J Psychiatry. 2018;175(4):359–69.

Pereira F, Mitchell T, Botvinick M. Machine learning classifiers and fMRI: a tutorial overview. Neuroimage. 2009;45(1 Suppl):S199-209.

Rojas DC, Peterson E, Winterrowd E, Reite ML, Rogers SJ, Tregellas JR. Regional gray matter volumetric changes in autism associated with social and repetitive behavior symptoms. BMC Psychiatry. 2006;6:56.

Carlisi CO, Norman LJ, Lukito SS, Radua J, Mataix-Cols D, Rubia K. Comparative multimodal meta-analysis of structural and functional brain abnormalities in autism spectrum disorder and obsessive-compulsive disorder. Biol Psychiat. 2017;82(2):83–102.

Wang M, Yu B, Luo C, Fogelson N, Zhang J, Jin Z, et al. Evaluating the causal contribution of fronto-parietal cortices to the control of the bottom-up and top-down visual attention using fMRI-guided TMS. Cortex. 2020;126:200–12.

Boxhoorn S, Bast N, Supèr H, Polzer L, Cholemkery H, Freitag CM. Pupil dilation during visuospatial orienting differentiates between autism spectrum disorder and attention-deficit/hyperactivity disorder. J Child Psychol Psychiatry. 2020;61(5):614–24.

Travers BG, Kana RK, Klinger LG, Klein CL, Klinger MR. Motor learning in individuals with autism spectrum disorder: activation in superior parietal lobule related to learning and repetitive behaviors. Autism Res. 2015;8(1):38–51.

Schmitt LM, White SP, Cook EH, Sweeney JA, Mosconi MW. Cognitive mechanisms of inhibitory control deficits in autism spectrum disorder. J Child Psychol Psychiatry. 2018;59(5):586–95.

Lin HY, Perry A, Cocchi L, Roberts JA, Tseng WI, Breakspear M, et al. Development of frontoparietal connectivity predicts longitudinal symptom changes in young people with autism spectrum disorder. Transl Psychiatry. 2019;9(1):86.

Wang Y, Zuo C, Xu Q, Hao L, Zhang Y. Attention-deficit/hyperactivity disorder is characterized by a delay in subcortical maturation. Prog Neuropsychopharmacol Biol Psychiatry. 2021;104:110044.

Faraone SV, Biederman J, Spencer T, Wilens T, Seidman LJ, Mick E, et al. Attention-deficit/hyperactivity disorder in adults: an overview. Biol Psychiat. 2000;48(1):9–20.

Kurth F, Levitt JG, Gaser C, Alger J, Loo SK, Narr KL, et al. Preliminary evidence for a lower brain age in children with attention-deficit/hyperactivity disorder. Front Psych. 2022;13:1019546.

Chouinard PA, Paus T. The primary motor and premotor areas of the human cerebral cortex. Neuroscientist. 2006;12(2):143–52.

Albajara Sáenz A, Villemonteix T, Van Schuerbeek P, Baijot S, Septier M, Defresne P, et al. Motor abnormalities in attention-deficit/hyperactivity disorder and autism spectrum disorder are associated with regional grey matter volumes. Front Neurol. 2021;12:666980.

Luo L, Chen L, Wang Y, Li Q, He N, Li Y, et al. Patterns of brain dynamic functional connectivity are linked with attention-deficit/hyperactivity disorder-related behavioral and cognitive dimensions. Psychol Med. 2023:53(14):6666–77.

Suskauer SJ, Simmonds DJ, Caffo BS, Denckla MB, Pekar JJ, Mostofsky SH. fMRI of intrasubject variability in ADHD: anomalous premotor activity with prefrontal compensation. J Am Acad Child Adolesc Psychiatry. 2008;47(10):1141–50.

Edden RA, Crocetti D, Zhu H, Gilbert DL, Mostofsky SH. Reduced GABA concentration in attention-deficit/hyperactivity disorder. Arch Gen Psychiatry. 2012;69(7):750–3.

Shaw P, Sharp WS, Morrison M, Eckstrand K, Greenstein DK, Clasen LS, et al. Psychostimulant treatment and the developing cortex in attention deficit hyperactivity disorder. Am J Psychiatry. 2009;166(1):58–63.

Norman LJ, Carlisi C, Lukito S, Hart H, Mataix-Cols D, Radua J, et al. Structural and functional brain abnormalities in attention-deficit/hyperactivity disorder and obsessive-compulsive disorder: a comparative meta-analysis. JAMA Psychiat. 2016;73(8):815–25.

Lim L, Marquand A, Cubillo AA, Smith AB, Chantiluke K, Simmons A, et al. Disorder-specific predictive classification of adolescents with attention deficit hyperactivity disorder (ADHD) relative to autism using structural magnetic resonance imaging. PLoS ONE. 2013;8(5):e63660.

Jung M, Tu Y, Park J, Jorgenson K, Lang C, Song W, et al. Surface-based shared and distinct resting functional connectivity in attention-deficit hyperactivity disorder and autism spectrum disorder. Brit J Psych. 2019;214(6):339–44.

Katuwal GJ, Cahill ND, Baum SA, Michael AM. The predictive power of structural MRI in autism diagnosis. Annual Int Conf IEEE Eng Med Biol Soc IEEE Eng Med Biol Soc Annual Int Confer. 2015;2015:4270–3.

Chang JC, Lin HY, Lv J, Tseng WI, Gau SS. Regional brain volume predicts response to methylphenidate treatment in individuals with ADHD. BMC Psychiatry. 2021;21(1):26.

DeCasien AR, Guma E, Liu S, Raznahan A. Sex differences in the human brain: a roadmap for more careful analysis and interpretation of a biological reality. Biol Sex Differ. 2022;13(1):43.

Luders E, Narr KL, Thompson PM, Woods RP, Rex DE, Jancke L, et al. Mapping cortical gray matter in the young adult brain: effects of gender. Neuroimage. 2005;26(2):493–501.

Sowell ER, Peterson BS, Kan E, Woods RP, Yoshii J, Bansal R, et al. Sex differences in cortical thickness mapped in 176 healthy individuals between 7 and 87 years of age. Cereb Cortex. 2007;17(7):1550–60.

Napolitano A, Schiavi S, La Rosa P, Rossi-Espagnet MC, Petrillo S, Bottino F, et al. Sex differences in autism spectrum disorder: diagnostic, neurobiological, and behavioral features. Front Psych. 2022;13:889636.

Ecker C, Andrews DS, Gudbrandsen CM, Marquand AF, Ginestet CE, Daly EM, et al. Association between the probability of autism spectrum disorder and normative sex-related phenotypic diversity in brain structure. JAMA Psychiat. 2017;74(4):329–38.

Bedford SA, Park MTM, Devenyi GA, Tullo S, Germann J, Patel R, et al. Large-scale analyses of the relationship between sex, age and intelligence quotient heterogeneity and cortical morphometry in autism spectrum disorder. Mol Psychiatry. 2020;25(3):614–28.

Dirlikov B, Shiels Rosch K, Crocetti D, Denckla MB, Mahone EM, Mostofsky SH. Distinct frontal lobe morphology in girls and boys with ADHD. NeuroImage Clin. 2015;7:222–9.

Nordahl CW. Why do we need sex-balanced studies of autism? Autism Res. 2023;16(9):1662–9.

Lee JK, Lee JM, Kim JS, Kim IY, Evans AC, Kim SI. A novel quantitative cross-validation of different cortical surface reconstruction algorithms using MRI phantom. Neuroimage. 2006;31(2):572–84.

Feng Y, Murphy MC, Hojo E, Li F, Roberts N. Magnetic resonance elastography in the study of neurodegenerative diseases. J Magn Reson Imaging. 2024;59(1):82–96.

Wang Y, Wu Y, Luo L, Li F. Structural and functional alterations in the brains of patients with anisometropic and strabismic amblyopia: a systematic review of magnetic resonance imaging studies. Neural Regen Res. 2023;18(11):2348–56.

You W, Luo L, Yao L, Zhao Y, Li Q, Wang Y, et al. Impaired dynamic functional brain properties and their relationship to symptoms in never treated first-episode patients with schizophrenia. Schizophrenia. 2022;8(1):90.

Luo L, Li Q, Wang Y, He N, Wang Y, You W, et al. Shared and disorder-specific alterations of brain temporal dynamics in obsessive-compulsive disorder and schizophrenia. Schizophrenia Bull. 2023:49(5):1387–98.

Li Q, Yao L, You W, Liu J, Deng S, Li B, et al. Controllability of functional brain networks and its clinical significance in first-episode schizophrenia. Schizophr Bull. 2023;49(3):659–68.

Ai Y, Li F, Hou Y, Li X, Li W, Qin K, et al. Differential cortical gray matter changes in early-and late-onset patients with amyotrophic lateral sclerosis. Cereb Cortex. 2024;34(1):bhad426.

Download references

Acknowledgements

The authors would like to express sincere gratitude to all the participants and investigators of the studies that were involved in this meta-analysis.

This study was supported by the National Natural Science Foundation of China (Grant No. 81801683 to LZC, 81820108018 to JAS and QYG, and 82027808 to QYG), Sichuan Science and Technology Program (2023YFS0226 to LZC and 23ZDYF2088 to YYL), Chengdu Technology Innovation Research and Development Project (2022-YF05-01590-SN), and National Key R&D Program of China (2022YFC2009900).

Author information

Wanfang You, Qian Li, and Lizhou Chen are co-first authors and contributed equally to this work.

Authors and Affiliations

Department of Radiology and Huaxi MR Research Center (HMRRC), Functional and Molecular Lmaging Key Laboratory of Sichuan Province, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, People’s Republic of China

Wanfang You, Qian Li, Lizhou Chen, Fenghua Long, Yaxuan Wang, Yufei Chen, John A. Sweeney, Qiyong Gong & Fei Li

Research Unit of Psychoradiology, Chinese Academy of Medical Sciences, Chengdu, 610041, Sichuan, People’s Republic of China

Wanfang You, Qian Li, Lizhou Chen, Fenghua Long, Yaxuan Wang, Yufei Chen, Qiyong Gong & Fei Li

Department of Radiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, 310016, Zhejiang, People’s Republic of China

Wanfang You

Department of Psychiatry, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, People’s Republic of China

Ning He & Yuanyuan Li

Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati, OH, 45219, USA

Robert K. McNamara, John A. Sweeney & Melissa P. DelBello

You can also search for this author in PubMed   Google Scholar

Contributions

FL conceptualized the article. WFY, QL, LZC, and FL drafted the manuscript. WFY, QL, LZC, NH, YYL, YXW, FHL, and YFC contributed to the literature search, data collection and analysis, as well as interpretation. WFY, QL, LZC, RKM, JAS, MPD, QYG, and FL contributed to interpretation of findings and critically revised the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Fei Li .

Ethics declarations

Ethics approval and consent to participate.

Not applicable.

Consent for publication

All authors read and approved the final manuscript.

Competing interests

MPD receives research support from national institutes of health (NIH), PCORI, Acadia, Allergan, Janssen, Johnson and Johnson, Lundbeck, Otsuka, Pfizer, and Sunovion. She is also a consultant, on the advisory board, or has received honoraria for speaking for Alkermes, Allergan, Assurex, CMEology, Janssen, Johnson and Johnson, Lundbeck, Myriad, Neuronetics, Otsuka, Pfizer, Sunovion, and Supernus. RKM has received research support from Martek Biosciences Inc, Royal DSM Nutritional Products, LLC, Inflammation Research Foundation, Ortho-McNeil Janssen, AstraZeneca, Eli Lilly, NARSAD, and NIH, and previously served on the scientific advisory board of the Inflammation Research Foundation. Other authors declare no potential conflicts of interest with regard to this manuscript.

Additional information

Publisher’s note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary Information

Additional file 1..

Supplementary methods of sensitivity, heterogeneity, publication bias, and meta-regression analyses. Table S1. PRISMA 2020 Checklist. Table S2. List of excluded studies that meet other inclusion criteria. Table S3. The checklist of imaging methodology quality assessment for all the articles included in the present meta-analysis. Table S4. Data sources of all public database studies included in the present meta-analysis. Table S5. Differences in cortical thickness between pure ADHD without comorbidity and TDC. Fig. S1. Results of cortical thickness differences between ASD and TDC. Fig. S2. Results of cortical thickness differences between ADHD and TDC.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/ ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

You, W., Li, Q., Chen, L. et al. Common and distinct cortical thickness alterations in youth with autism spectrum disorder and attention-deficit/hyperactivity disorder. BMC Med 22 , 92 (2024). https://doi.org/10.1186/s12916-024-03313-2

Download citation

Received : 01 September 2023

Accepted : 22 February 2024

Published : 04 March 2024

DOI : https://doi.org/10.1186/s12916-024-03313-2

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

  • Surface-based morphometry

BMC Medicine

ISSN: 1741-7015

essay on attention deficit disorder

IMAGES

  1. Is ADHD a Real Disorder? Free Essay Example

    essay on attention deficit disorder

  2. A Detailed Review Of Attention Deficit Hyperactivity Disorders (ADHD

    essay on attention deficit disorder

  3. (PDF) Teaching Writing to Students With Attention Deficit Disorders and

    essay on attention deficit disorder

  4. 📌 Research Paper on Attention Deficit Disorder

    essay on attention deficit disorder

  5. Attention Deficit Hyperactivity Disorder

    essay on attention deficit disorder

  6. (PDF) ATTENTION DEFICIT DISORDERS AMONG ADULT LEARNERS: CAUSES

    essay on attention deficit disorder

VIDEO

  1. What Is ADHD

  2. Informative Speech-Attention Deficit Hyperactivity Disorder(Full Speech)

  3. Attention Deficit Hyperactivity Disorder vs Autism

  4. A.D.H.D. (Attention Deficit Hyperactivity Disorder)

COMMENTS

  1. My Battle with ADHD: Personal Essay

    Breaking Barriers: My Battle with ADHD. In a prize-winning essay about overcoming obstacles, a child with attention deficit disorder explains the effects of ADHD on his life. From enlisting the help of family members to keeping a journal, this is how Jack Prey manages his diagnosis. By Jack Prey Verified Updated on May 15, 2020.

  2. ADHD Is My Superpower: A Personal Essay

    A Warp Speed Brain. To have ADHD means that your brain is an engine that's constantly running at high speed. It basically never stops wanting to process information at a high rate. The "attention" part is just an observable set of behaviors when an ADHD person is understimulated. This is also part of why I now openly associate as ...

  3. ADHD Essay Writing Help: 18 Strategies for Better School Writing

    Studies suggest that more than half of children with attention deficit disorder (ADHD or ADD) struggle with writing.These students may have an overflow of creative ideas, but often struggle when it comes to getting these ideas onto paper.. Children with ADHD have a hard time getting started — and following through — on writing assignments because they have difficulty picking essay topics ...

  4. ADHD: Current Concepts and Treatments in Children and Adolescents

    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 ...

  5. Attention Deficit Hyperactivity Disorder

    Attention Deficit-Hyperactivity Disorder (ADHD) is a psychiatric condition that has long been recognized as affecting children's ability to function. Individuals suffering from this disorder show patterns of developmentally inappropriate levels of inattentiveness, hyperactivity, or impulsivity. Although there used to be two different diagnoses of Attention Deficit Disorder vs. Attention ...

  6. Writing Strategies for Students With ADHD

    Here are some practical solutions for teachers to encourage, motivate, and focus their students on writing process. 1. Difficulty Concentrating on Assignment. Research proves that ADHD doesn't result in less intelligence, but rather in difficulties controlling emotions, staying motivated, and organizing the thoughts.

  7. Cognitive Psychology and Attention Deficit Disorder Essay

    Attention-deficit disorder (ADD) is a neurobehavioural developmental problem that is increasingly becoming a major problem in today's world than it was in yesteryears. The trend at which more and more people are being with ADD is worrying. This disorder is not age-bound as it affects both children and adults. Principally the illustration of ...

  8. ADHD: Reviewing the Causes and Evaluating Solutions

    1. Introduction. Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder (NDD) presenting with inattention, hyperactivity, and impulsivity. It can be classified in three subtypes, depending on the intensity of the symptoms: predominantly inattentive, predominantly hyperactive-impulsive, and combined [ 1, 2 ].

  9. Attention-Deficit Hyperactivity Disorder (ADHD), Essay Example

    Symptoms, Diagnosis and Development. Attention-Deficit Hyperactivity Disorder (ADHD) manifests itself with the symptoms of impulsiveness, inability to focus or concentrate impulsivity and hyperactivity. It is a chronic neurobehavioral syndrome further classified as a psychiatric disorder. Often people diagnosed with this disorder tend to have ...

  10. Writing Problems Common for Students With ADHD

    Essays and reports that require students to communicate what they know on paper factor more prominently into the curriculum. It is no wonder that writing can create such anxiety in students with ADHD. ... Mokobane M, Pillay BJ, Meyer A. Fine motor deficits and attention deficit hyperactivity disorder in primary school children. S Afr J ...

  11. Attention Deficit Disorder Essays (Examples)

    Attention Deficit Disorder According to the American Psychiatric Association (APA) (1994), Attention Deficit Hyperactivity Disorder (ADD or ADHD) is a diagnosis given to children and adults who display certain characteristic behaviors on a consistent basis over an extended period of time. The most common behaviors that characterize ADD include inattention, hyperactivity, and impulsivity.

  12. Understanding and Supporting Attention Deficit Hyperactivity Disorder

    Children with Attention Deficit Hyperactivity Disorder (ADHD) are more at risk for academic underachievement compared to their typically developing peers. Understanding their greatest strengths and challenges at school, and how these can be supported, is vital in order to develop focused classroom interventions. Ten primary school pupils with ADHD (aged 6-11 years) and their teachers (N = 6 ...

  13. 162 ADHD Topics for Essays & Research Papers

    ADHD (attention deficit hyperactivity disorder) is a very common condition nowadays. It is definitely worth analyzing. In your ADHD essay, you might want to focus on the causes or symptoms of this condition. Another idea is to concentrate on the treatments for ADHD in children and adults.

  14. What is ADHD?

    Types. There are three different ways ADHD presents itself, depending on which types of symptoms are strongest in the individual: Predominantly Inattentive Presentation: It is hard for the individual to organize or finish a task, to pay attention to details, or to follow instructions or conversations. The person is easily distracted or forgets details of daily routines.

  15. Attention Deficit Hyperactivity Disorder (ADD / ADHD)

    ADHD is divided into three special types; overbearingly hyperactive and impulsive. majorly inattentive and. A blend of hyperactivity, impulsiveness and inattention. Overly hyperactive-impulsive ADHD children may also exhibit lack of attention while the inattentive ADHD ones may also show symptoms of hyperactivity and impulsiveness.

  16. Attention Deficit Disorder Essay

    Attention Deficit Hyperactivity Disorder (ADHD) Essay. Attention Deficit Hyperactivity Disorder, normally abbreviated as ADHD, is a disorder in which a person has trouble paying attention and focusing on tasks, tends to act without thinking and has trouble sitting still. This condition may begin in early childhood and continue into adulthood.

  17. Attention Deficit Hyperactivity Disorder In The Classroom

    Impulsivity is an impaired ability to control one's own behavior. (Smith and Tyler, 2010) Literature Review. Attention deficit hyperactivity disorder is a labeled given to students that have a serve problem with attention and impulsiveness. Male children are the ones usually diagnosed with ADHD. ADHD usually effect boys more often than girls.

  18. Essay about Attention Deficit Disorder

    Essay about Attention Deficit Disorder. Better Essays. 3040 Words; 13 Pages; 6 Works Cited; Open Document. Attention Deficit Disorder Five year old Danny is in kindergarten. It is playtime and he hops from chair to chair, swinging his arms and legs restlessly, and then begins to fiddle with the light switches, turning the lights on and off ...

  19. Attention Deficit Hyperactivity Disorder (ADHD)

    Popular Essay Topics. Attention Deficit Hyperactivity Disorder (ADHD) is a neurodevelopment disorder that is commonly seen amongst children, characterized by impulsive and hyperactive symptoms that can seriously affect day-to-day functioning. Beyond its obvious symptoms, this disorder affects a child's academic performance, social ...

  20. ADHD essay

    school paper adhd running head: attention deficit hyperaxtivity disorder attention deficit hyperactivity disorder, diagnosis and treatment park university. Skip to document. University; High School. Books; Discovery. ... Essays For Scholarships; Week 3 Summative Assessment; ADHD Paper - Grade: A;

  21. Essay on Attention Deficit Hyperactivity Disorder

    According to the American Psychiatric Association, Attention Deficit Hyperactivity Disorder is characterized by pervasive and developmentally inappropriate difficulties with attention, impulsivity, and hyper activity. These students frequently have difficulties following classroom rules and can show aggression, they are also more likely to be ...

  22. NIH researchers identify brain connections associated with ADHD in

    They found that youth with ADHD had heightened connectivity between structures deep in the brain involved in learning, movement, reward, and emotion (caudate, putamen, and nucleus accumbens seeds) and structures in the frontal area of the brain involved in attention and control of unwanted behaviors (superior temporal gyri, insula, inferior ...

  23. Psychology: Attention Deficit and Hyperactivity Disorder Essay

    Exclusively available on IvyPanda. Attention Deficit/Hyperactivity Disorder (ADHD) is a common illness for children though it can also be found in adults. There are three types of this disorder: the hyperactive-impulsive type (HI), the inattentive type (PI), and the combined type. Notably, the third type is the most common (Mash & Wolfe, 2013).

  24. NIH Researchers Identify Brain Connections Associated With ADHD ...

    They found that youth with ADHD had heightened connectivity between structures deep in the brain involved in learning, movement, reward, and emotion (caudate, putamen, and nucleus accumbens seeds) and structures in the frontal area of the brain involved in attention and control of unwanted behaviors (superior temporal gyri, insula, inferior ...

  25. Assessing the Contribution of Measures of Attention and ...

    Attention and executive function (EF) dysregulation are common features of neurodevelopmental, mental health, and neurologic disorders, such as Attention Deficit Hyperactivity Disorder (ADHD), Autism (Boxhoorn et al., 2018), traumatic brain injury (Bonnelle et al., 2011), and obsessive compulsive behavior (Koch and Exner, 2015), as either primary (part of diagnosis) or secondary (common in the ...

  26. Guanfacine for the Treatment of Attention-Deficit/Hyperactivity

    If the address matches an existing account you will receive an email with instructions to reset your password.

  27. Attention-Deficit/Hyperactivity Disorder Medications and Long-Term Risk

    This case-control study found that long-term exposure to ADHD medications was associated with an increased risk of CVDs, especially hypertension and arterial disease. These findings highlight the importance of carefully weighing potential benefits and risks when making treatment decisions about long …

  28. Attention Deficit Hyperactivity Disorder in Children Essay

    Diagnostic Information (Psychopathology) The child's patterns of inattention, physical agitation, lack of focus in studies, and restlessness attribute to the diagnosis of Attention Deficit Hyperactivity Disorder (ADHD). Indeed, the purposeless distractibility and reduced attention span of Jonathan attribute to the preliminary symptoms of ADHD ...

  29. Common and distinct cortical thickness alterations in youth with autism

    Search strategy and study inclusion. The present study was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (see Additional file 1: Table S1).A systematic search was conducted for peer-reviewed English language publications in PubMed, Web of Science, Embase, and Science Direct from inception to 8 December 2023.

  30. Environmental pollution and attention deficit hyperactivity disorder: A

    There is already knowledge of the extensive risk factors for attention deficit hyperactivity disorder (ADHD) and recent studies suggest that environmental pollution may contribute to an increase in the incidence of the disorder. The aim of our study was to perform a systematic review and meta-analysis of the risk of ADHD in people younger than 18 years old after exposure to environmental ...