The ADHD Brain
It has definitely been a challenge, summarizing the vast amount of studies covering the pathophysiology of the ADHD brain. Yet, the answer may lay within these 8 neuroimaging pictures by Faraone, S.V. et al. (2015) in his study 'Brain mechanisms in attention-deficit/hyperactivity disorder'. Images below.
Firstly why is neuroimaging so important when determining the pathophysiology of ADHD?
Neuroimaging provides a clear picture of functional change (pathophysiology) within ADHD brains. Through these studies/images we have learned, that even though environmental factors and genetics also play role in ADHD. The ADHD brain is significantly different to neuro-typical (non-ADHD) brains, in terms of brain structure and functional connectivity (wiring).
This information has a huge implication for the millions of struggling families and adults living with ADHD. The implication being that ADHD is not due to bad parenting or adults simply having no life organisational skills. Certainly ADHD symptoms can be exacerbated by our external environment, but these images below demonstrate that there is a neurological basis behind ADHD.
ADHD is considered a neurological disorder, manifesting as (but not restricted to) symptoms such as hyperactivity, distractibility, and poor impulse control.
ADHD also falls under the umbrella term of Neurodiversity, which basically means neurologically different. Neurodiversity encompasses a wide range of neurological conditions, namely Autism Spectrum Disorders (ASD), ADHD, Dyslexia, Dyscalculia, Dyspraxia, Tourette's, OCD plus others.
Neurodiversity is considered the conclusion of a natural and normal variation in the human genome. One who thinks and acts differently to the norm, and who should be respected as any other human being who is different. Symptoms can be addressed if it causes a issue in the person's daily functionality.
Journalist Harvey Blume first wrote about neurodiversity in a 1998 article published in the Atlantic. Blume said, "Neurodiversity may be every bit as crucial for the human race as biodiversity is for life in general. Who can say what form of wiring will prove best at any given moment?" And who can say?! We will cover more on the exciting possibilities of Neurodiversity in part 2 of this series.
Brain mechanisms in attention-deficit/hyperactivity disorder
Figure (a) & (b) - present the main regions implicated by functional and structural neuroimaging studies.
Figure (c) - shows these regions being connected by neural networks rich in two neurotransmitters - Dopamine & Noradrenalin. ADHD medication treats ADHD by regulating the activity of these neurotransmitters.
Figure (d) - represents two functional networks.
The Corticocerebellar Network - Regulator of complex motor skills & plays a possible role in the regulation of cognitive functions.
The Executive Control Network - Regulates behavior by connecting the dorsal striatum and the dorsolateral prefontal cortex. This pairing is necessary for inhibitory control, self-regulation, working memory and attention.
Figure (e) - illustrates the Reward Network that connect the ventral striatum with prefrontal cortex. This Reward Network regulates how we perceive and value rewards and punishments. This network is thought to play a significant role on substance abuse addictions. Which is why, the ADHD community are at a particularly high risk for addictions.
Figures (f), (g) & (h) - highlights less understood additional regions in the pathophysiology of ADHD. A primary role for these regions is the regulation of the Default Mode Network (DMN). This network is active, when a person isn't focused on a task. While in this mode the brain will zone out, day dream, mind wander to past memories and actually future plan. A disruption in the DMN is implicated not only in ADHD but other disorders such as ASD and Alzheimer's. This may explain why Alzheimer's patients respond so well to an external environment, which reflects the patient's internal memories. This externalization can be expressed through the music of their youth and objects/photographs from their past. It would also explain the rich imagination and creativity found in people with ADHD and ASD.
Typically we see a continuous dynamic interaction between the DMN (thinking about a great idea) and the Executive Network (making that idea a reality). However when both networks are dis-regulated, the natural communication style of expressing ideas/concepts becomes complicated, this is especially true for autistic individuals. It may also indicate why people with ADHD can often feel misunderstood and easily frustrated, when required to explain their vision or give an opinion.
A classic example of this would be Steve Jobs (founder of Apple), who was a rumored ADHDer. It has been well documented how Jobs would unleash a reign of terror on his poor employees, who questioned his 'vision'. Personally I don't believe that this was an issue of Jobs being a proud or arrogant individual but of an inability to express his vivid and surreal internal world in any other way, than how he saw it. ADHDers find it very difficult to find other ways, to make their ideas more easily understandable. The frustration felt by many people with ADHD, comes down to a communication issue which has both internal and external implications. An ADHD child will thrive with an educator who doesn't presume the ideas/actions of an ADHD child is wrong, just because they don't fit inside a box, a curriculum or a text book. A teacher who has mastered the art of listening, paraphrasing and summarising with enthusiasm is exactly the validation and encouragement an ADHD child needs to express themselves more clearly and to get that child's plan into action.
Faraone, S. V. et al. (2015) Attention-deficit/hyperactivity disorder Nat. Rev. Dis. Primers doi:10.1038/nrdp.2015.20 ; http://rdcu.be/gYyV
Armstrong, Thomas. The Power of Neurodiversity: Unleashing the Advantages of Your Differently Wired Brain. Cambridge, MA: DaCapo Lifelong/Perseus Books, 2011.
Qiu MG, Ye Z, Li QY, et al. Changes of brain structure and function in ADHD children. Brain Topogr 2011;24:243-52.