If you search for “What is ADHD?”, the top results will be from authorities like the Center for Disease Control (CDC) and the American Psychiatric Association. Each of these sources provides a wordy description of Attention-deficit/hyperactivity disorder (ADHD) according to the Diagnostic and Statistical Manual of Mental Disorders (DSM).
The problem with that is that the DSM doesn’t tell you what ADHD is, only what it does. And unfortunately the term ADHD comes from that same list of behaviors. This means that both the name and the diagnostic symptoms fail to provide a meaningful description or any hint about the cause. But there’s a good reason for that: ADHD is not perfectly understood.
So where can we find an accurate and authoritative description of what ADHD is? Well, short of digging into the scientific research and devouring piles of books on ADHD, we haven’t found one. That’s pretty much why we decided to put this together. Because we care enough to dig into the research, read every book we can get our hands on, and even go through dedicated training. Obsessed? Damn skippy! And proud of it.
So, What IS ADHD?
ADHD is a neurobiological condition that causes some areas of the brain to develop differently than most human brains.
Translation: our brains work differently than most people’s because they grew that way.
They’ve unequivocally proven that ADHD is genetic. Researchers are still working hard to identify the various causes. Wait, causes? There’s more than one? Yep, that’s right. ADHD has a 70 to 80% heritability rate in both children and adults. But there are a lot of different genes involved and the characteristics those genes cause depend heavily on environmental factors. The effect of the environment on our genes, called epigenetics, is why we each have our own unique cocktail of ADHD characteristics. There’s a saying in the ADHD community “once you’ve seen one person with ADHD, you’ve seen ONE person with ADHD”.
Patients with ADHD show marked variation in profiles of symptoms, impairments, complicating factors, neuropsychological weaknesses and underlying causes.
The different genetic causes also explain why about 30% of people with ADHD (1) don’t benefit from stimulant medication. They still have challenges with hyperactivity and attention, but the distinction is that these symptoms don’t come from the gene impacting the production of neurotransmitters.
Which Parts of ADHD Brains Work Differently?
While neurologists haven’t figured out everything that’s going on with ADHD brains, they have identified the main areas involved. To emphasize, not everyone with ADHD will have all these areas affected. It depends on your genes and the environment in which your brain developed.
There is a lot of information to dive into with the neurology of ADHD but here’s a high-level overview to start with. Let’s do a chart! Think of this as the buffet of ADHD neurological impacts.
Executive Control and Corticocerebellar Networks
These executive control and corticocerebellar networks control executive functioning: planning, goal-directed behavior, inhibition, working memory, and flexible adaptation to context. These areas are under-activated and have lower internal connectivity in individuals with ADHD. In particular, the parietal cortex handles the orientation of attention. The dorsolateral prefrontal cortex (PFC) handles working memory (ever forget the one-time security code as soon as you looked up to type it in a website?). And the ventromedial PFC takes care of complex decision-making and strategic planning.
The frontostriatal circuit is made up of the ventral and dorsal anterior cingulate cortices which support the ability to regulate emotions (2) and the cognitive components of executive control. The basal ganglia are known for the control of movement, behavior, and emotions. (3) Neuroimaging studies of patients with ADHD show structural and functional abnormalities in these structures, as well as the amygdala and cerebellum.
The reward system is a center of the brain network that responds to anticipation and receipt of reward (think motivation). Behavioral and neural responses to reward are abnormal in ADHD. As a result, those with an ADHD brain prefer immediate over delayed rewards. Additionally, rewards that are closer seem more rewarding than ones that are far away.
The alerting network Supports attentional functioning and is weaker in individuals with ADHD. This is the network responsible for allowing us to tune out or disregard stimuli (squirrel!) that aren’t relevant to our current activity.
Default-Mode Network (DMN)
The human brain has two modes: the DMN and the Task Positive Networks (TPN). The TPN is engaged for active tasks (such as driving) and the brain reverts to the DMN when there is no activity. Under normal operation, only one of these networks is active at a time. (4) In ADHD brains, they’ve shown that is often not the case and that we can have both competing for processing resources. Have you ever been driving and suddenly “woke up” or pulled into your driveway without remembering the drive home? That’s your TPN driving and your DMN occupying your attention. Dr. Ned Hallowell refers to the DMN as the Demon because this is the system that can cause negative thought spirals and rumination.
Neurotransmitter circuits are not included in the chart because they run throughout the brain. The dopamine and noradrenergic system (norepinephrine) play a large role in the other systems we’ve discussed and, like many of the other systems mentioned, are under-active in ADHD. The dopamine system has an important role in planning and initiation of motor responses, activation, switching, reaction to novelty, and processing of reward. The noradrenergic system influences arousal modulation (emotional response), the signal-to-noise ratio in cortical areas, physical or psychological state-dependent (e.g. hunger, intoxication, physical location, stress) (5) cognitive processes, and cognitive preparation of urgent stimuli (squirrel!).
Wow. How Could Anyone Get by with ADHD?
Now here’s the kicker. In certain situations, our brains work almost completely as a neurologist would expect of any human brain, and in some ways better. In addition to each individual’s particular genes, this “situational variability” is what makes ADHD challenging to diagnose. It’s also the primary cause of our own doubts about having ADHD, even after we’ve been diagnosed. “But I did this just fine last week! Why can’t I do it now?”
Some of you were diagnosed with ADHD a while ago, were given a prescription, and sent on your way with no education about what the diagnosis meant. Or you were diagnosed and forgot about it (no really, this happens!). And some of you are probably reading this because you’re on the fence about whether you have ADHD, and whether you want to be assessed. You might have seen all of the ADHD-related videos and memes on social media and thought, “Yes, that’s me!”. But then you saw the list of diagnostic criteria and began to have doubts.
Situational variability means that those diagnostic symptoms don’t happen all the time. And the different presentations of ADHD mean that you won’t experience all the symptoms or each of them to the same degree. The difference between an ADHD diagnosis and “everyone’s a little forgetful from time to time”, is one of the last criteria. “There is clear evidence that the symptoms interfere with, or reduce the quality of, social, school, or work functioning.” When ADHD affects school performance or results in routinely getting fired from jobs, the impact on quality of life is obvious. Less obvious are the situations in which our compensating strategies successfully keep us “in the game” at school or work. But those strategies can come with a mental health cost that eventually gets too high to pay.
Whether you’ve known about ADHD for a while or you’re at the start of your journey, we’re obsessed with making sure you get the information you need. Because understanding your ADHD brain makes it possible to adapt your environment and habits to work with your brain.
Unless otherwise cited, all facts and scientific information on this page are referenced from:
Faraone, S., Asherson, P., Banaschewski, T. et al. Attention-deficit/hyperactivity disorder. Nat Rev Dis Primers 1, 15020 (2015). https://doi.org/10.1038/nrdp.2015.20
Colwell, C. (2021, July 21) Is Leaky Thalamus to Blame for ADHD? HCPLive. https://www.hcplive.com/view/is-leaky-thalamus-to-blame-for-adhd
Schweizer, S., Grahn, J., Hampshire, A., Mobbs, D., Dalgleish, T. Training the Emotional Brain: Improving Affective Control through Emotional Working Memory Training. Journal of Neuroscience. 33 (12) 5301-5311. Published 20 March 2013. DOI: 10.1523/JNEUROSCI.2593-12.2013
Lanciego J.L., Luquin N, Obeso J.A. Functional neuroanatomy of the basal ganglia. Cold Spring Harb Perspect Med. 2012;2(12):a009621. Published 2012 Dec 1. doi:10.1101/cshperspect.a009621
- Hallowell, E. M., & Ratey, J. J. (2021). ADHD 2.0. Ballantine Books.
- American Psychological Association. (2021, July 21). State-Dependent Memory. APA Dictionary of Psychology. https://dictionary.apa.org/state-dependent-memory