Why Are Stimulants Used to Treat Hyperactivity?

By Annette Miller: For Entire Post, Go Here…

The neuroscience of ADHD reveals counterintuitive realities.

At 29 years old, sitting in a poorly lit graduate program classroom, I suddenly saw why my lifetime of struggles with depression didn’t fit neatly into a single circle.

“Maybe I do have ADHD,” I thought.

By this time, I was independently learning about the translational research that connects basic cognitive research with applied clinical practice. I’d previously learned the basics of how the brain works. I knew my stuff. My undergraduate education is in Behavioral Neuroscience and I did animal research for my senior thesis project.

I’ve lost count of how many times I have been tested on basic neurobiological concepts. The synaptic cleft, myelinated sheath, dopaminergic pathways, and cannabinoid receptors. Ionized channels. Functions of the amygdala, and so on and so on.

What I did not yet know was that certain neurobiological interactions can have a camouflaging effect.

What does this mean?

Symptoms are categorized in the process of assessing a client’s overall functioning. This can lead to unintentional symptom misattribution and misdiagnosis of mental health disorders. In fact, ADHD is frequently — erroneously — diagnosed as Major Depressive Disorder or various anxiety disorders. More confusing still, ADHD can (and often does) co-exist with these secondary disorders.

That was my experience.

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This Venn diagram details the neuroscience underlying individual symptoms of depression, anxiety, and ADHD.

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