ADHD: It’s all in your head

That’s where your brain is.

ADHD is a neurodevelopmental disorder that impacts 7.2% of children(1) and 3.4% of adults (2). As of 2020 that is 164 million children and 187 million adults.

What causes ADHD? 

In most cases, it’s due to genetics. The majority of ADHD cases are due to the individual inheriting genes associated with neurological dysfunction, which hinders the body's communication system. Brain trauma and/or infection has been linked to ADHD. Environmental and social factors can also have some impact on a child's likelihood of developing symptoms of ADHD (3).

There are physical differences in certain regions of ADHD brains, particularly in those associated with the chemical transmitters dopamine and norepinephrine (also known as noradrenaline) (5,6).

Structural Differences in ADHD Brains: 

  1. A lower density of grey matter, which is involved in muscle control, sensory perception, memory, emotions, speech, decision-making, and self-control (5).
  2. White matter abnormalities which affects learning and brain function, as white matter relays messages throughout the brain (6). 
  3. Cortical differences, including delayed cortical maturation in ADHD children and reduced cortical thickness in adults. These abnormalities hinder age-appropriate attention, behavior, sensation, memory, and visual processing.
  4. Reduced total brain volume (5). 

Functional Differences 

Brain imaging studies on ADHD individuals have shown underactive parts of the brain associated with executive function, attention, working memory, and decision-making, as well as within the areas responsible for mediating motor, cognitive, and behavioral functions (5).

ADHD brains also have an overly active default mode network while performing tasks. The default mode network becomes more active when people aren’t busy, and it allows us to daydream, reflect, recall memories, evaluate our life, and envision the future. For neurotypical brains, this undirected thinking slows down when someone is engaged in a task to allow them to focus. ADHD brains cannot turn down the dial on their default mode network which leaves many of us restless, distracted, and agitated.

Chemical Differences 

The brain sends messages throughout the body, allowing you to think, move, and function. These messages are sent through neurons with the assistance of neurotransmitters.

ADHD brains don’t release enough of certain transmitters, or restart them too quickly for a connection to be made. Because of this, the messages being sent aren't received as easily as those in neurotypical brains (8). It is because of this delay that people with ADHD struggle with attention and motivation. Though they may fully intend to complete a task or engage in a conversation, the chemical resources required to do so aren’t always available.

Treatment 

The reason why many children with ADHD may grow up to be considered neurotypical adults is due to a lag in age-appropriate brain development. As children, their ADHD brains fall well outside of the range of normal growth, but eventually, they catch up. A third of ADHD children do not reach this point, growing into ADHD adults.

Adult ADHD cannot be cured, but it can be managed.

Diet, exercise, positive psychology, therapy, and supplements can all help to reduce symptoms and improve overall health, but it must be stressed that this is a neurodevelopmental disorder, these lifestyle changes, though helpful, are not always sufficient in managing ADHD symptoms.

Pharmacological treatments for ADHD improve symptoms by increasing the amount of dopamine and norepinephrine available, giving your nervous system the fuel it needs to relay information. While medications do not change the structure of your brain they do improve symptoms, giving your brain the resources it needs to better send and receive messages. Treatments include both stimulant and non-stimulant medications (9).

Stimulants such as methylphenidate (Ritalin, Concerta) and amphetamine (Adderall, Mydayis) are most commonly prescribed to treat ADHD. They reduce ADHD symptoms by increasing dopamine levels, improving the brain’s ability to communicate within itself (9).

Non-stimulant treatment for ADHD includes atomoxetine (Strattera) and guanfacine (Intuniv, Tenex.). Atomoxetine (Strattera) increases the amount of norepinephrine (a chemical messenger) available to the brain, improving concentration, hyperactivity and impulsivity. Guanfacine (Intuniv, Tenex.) improves central noradrenergic signaling, which enhances working memory and reduces emotional dysregulation, aggression, and hyperarousal (9). The sympathetic nervous system is responsible for the fight, flight, and freeze responses, and guanfacine slows down this system, preventing you from perceiving threats incorrectly.


The next time someone tells you your ADHD is ‘All in your head’ feel free to link them to this article. 

Author: Teish Robert
Editor: Nathalie Goyette


References 
1. Thomas, R., Sanders, S., Doust, J., Beller, E., & Glasziou, P. (2015). Prevalence of attention  deficit/hyperactivity disorder: a systematic review and meta-analysis. Pediatrics, 135(4), e994–e1001. https://doi.org/10.1542/peds.2014-3482 

2. Fayyad, J., De Graaf, R., Kessler, R., Alonso, J., Angermeyer, M., Demyttenaere, K., De Girolamo, G., Haro, J. M., Karam, E. G., Lara, C., Lépine, J. P., Ormel, J., Posada-Villa, J., Zaslavsky, A. M., & Jin, R. (2007). Cross-national prevalence and correlates of adult attention-deficit hyperactivity disorder. The British journal of psychiatry: the journal of mental science, 190, 402–409. https://doi.org/10.1192/bjp.bp.106.034389 

3. American Psychiatric Association. Attention-deficit and disruptive behavior disorders. In: 
Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Association; 2013. 

4. Quinn, P. O., & Madhoo, M. (2014). A review of attention-deficit/hyperactivity disorder in 
women and girls: uncovering this hidden diagnosis. The primary care companion for CNS disorders, 16(3), PCC.13r01596. https://doi.org/10.4088/PCC.13r01596 

5. Cortese, S., Kelly, C., Chabernaud, C., Proal, E., Di Martino, A., Milham, M. P., & 
Castellanos, F. X. (2012). Toward systems neuroscience of ADHD: a meta-analysis of 55 fMRI studies. The American journal of psychiatry, 169(10), 1038–1055. https://doi.org/10.1176/appi.ajp.2012.11101521 

6. Bu, X., Liang, K., Lin, Q., Gao, Y., Qian, A., Chen, H., Chen, W., Wang, M., Yang, C., & 
Huang, X. (2020). Exploring white matter functional networks in children with attention-deficit/hyperactivity disorder. Brain communications, 2(2), fcaa113. https://doi.org/10.1093/braincomms/fcaa113 

7. Purper-Ouakil, D., Ramoz, N., Lepagnol-Bestel, A. M., Gorwood, P., & Simonneau, M. 
(2011). Neurobiology of attention deficit/hyperactivity disorder. Pediatric research, 69(5 Pt 2), 69R–76R. https://doi.org/10.1203/PDR.0b013e318212b40f 

8. Wu, J., Xiao, H., Sun, H., Zou, L., & Zhu, L. Q. (2012). Role of dopamine receptors in
ADHD: a systematic meta-analysis. Molecular neurobiology, 45(3), 605–620. https://doi.org/10.1007/s12035- 012-8278-5 

9. Kolar, D., Keller, A., Golfinopoulos, M., Cumyn, L., Syer, C., & Hechtman, L. (2008). 
Treatment of adults with attention-deficit/hyperactivity disorder. Neuropsychiatric disease and treatment, 4(2), 389–403. https://doi.org/10.2147/ndt.s6985