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.
Original image by Annette Miller.
This Venn diagram details the neuroscience underlying individual symptoms of depression, anxiety, and ADHD.
It begs an obvious question: “What needs stimulation?”
Seeing a version of it for the first time was a huge “aha!” moment. As an admittedly precocious early-career psychotherapist, I thought I knew everything I needed to understand about neuroscience fundamentals. Wrong. Even as a clinical psychology research-practitioner in training, this was a whole wormhole I had no idea existed, much less explained my own experience. The complexity of these brain chemicals and how they interact poses real challenges.
Even in my assessment, my strong academic achievements and career history (performance ability) were used to rule out an ADHD diagnosis while overlooking things like:
procrastination, time blindness, and chronic lateness
difficulty getting focused during tests, especially in large lecture halls
constant need for caffeine and naps, despite ample sleep
near-constant fidgeting or doodling during lectures
unbearable boredom in subjects I did not love
interrupting and inappropriate talkativeness in group discussions
It would be a big lie to say I enjoyed the Biological Bases of Behavior course while earning my Masters in Counseling Psychology. The teacher was bizarrely authoritarian to be teaching a graduating cohort of effusive, congenial, soon-to-be psychotherapists. But classroom dynamics aside, I learned about the entanglements of various neurochemicals in this class — and it blew my mind for very personal reasons.
The dangers of misdiagnosis
It is imperative to consult a licensed professional mental health provider for assessment and treatment. Misdiagnosis can have a range of implications. The worst is inappropriate treatment.
Beyond psychotherapy, misdiagnosis is particularly dangerous when psychopharmacological treatments are introduced. Examples of dangerously misprescribing:
Erroneously prescribing antipsychotics can cause major and irreversible side effects. This is common in the misdiagnosis of schizophrenia.
Lithium can be extremely harmful to patients who do not, in fact, have Bipolar Disorder.
Misdiagnosing ADHD as depression results in the wrong neurotransmitters being targeted or activated.
The neuroscience You might reasonably expect hyperactivity would demand medication with calming properties — the opposite of stimulants. It is counterintuitive then that a person with Attention Deficit Hyperactivity Disorder (ADHD) might need stimulant medication of some sort. It begs an obvious question: “What needs stimulation?” You’ve probably heard of neurotransmitters. They are critical messengers within the brain, influencing everything from mood to sleep cycles. These electrochemical chatty Cathys are also the lead actors on the dynamic stages of our mental health. One particular subtype of neurotransmitter — monoamines — is key to explaining why stimulants are used in treatment for ADHD, but not for depression. The functions of monoamines range from basic, life-sustaining activities to more evolved, frontal-lobe functions:
Noradrenaline — alertness, concentration, energy
Dopamine — pleasure, reward, reinforcement
Seratonin — sex drive, sleep, appetite, memory
Fascinating, recent research on monoamines suggests many species of animals use serotonin, dopamine, and noradrenaline similarly. Even fruit flies appear to use these types of cells in “essential physiological roles…learning and memory, aggression, mating behaviors, and reproduction, stress response, locomotion, and collective social behaviors,” according to the editors of a recent article on the role of monoamines in modulating behavior.
Stimulants vs. SSRIs
The reason stimulants are the front-line, gold-standard treatment for ADHD is because Dopamine is understood to play the biggest role in functional impairment. Mood and motivation dysregulation, for example, are major issues. But stimulants are named for their Dopamine-circulating properties in the brain. People with ADHD don’t have enough Dopamine circulating naturally in the brain. There’s probably one other thing you’ve heard of — SSRIs. This is short for Selective Seratonin Reuptake Inhibitor. Typically prescribed for depressive disorders, SSRIs are named for their Seratonin-circulating properties in the brain. People with depression don’t have enough Seratonin circulating naturally in the brain. If we put these two bits of information together, we see Seratonin and Dopamine are key players in Depression and ADHD, respectively.
Consequently, medication is an appropriate long-term treatment plan and considered the gold standard in mainstream American medicine.
While you can absolutely adopt healthier habits and get better and better at managing your symptoms, it may feel like rolling a rock uphill without medication. My personal experience with medication is that it has helped make new habits and routines immensely easier. It hasn’t been a magic fix, by any means, but it has allowed me to make the changes I wanted to make and maintain.
By contrast, episodes of Major Depression may call for antidepressants, but because it is a temporary problem, medication is not typically required long-term. (I have Chronic Depressive Disorder, which is why I do take antidepressants long-term. Sometimes I have the fun privilege of experiencing ADHD, CDD, and Major Depressive episodes simultaneously! Yay!)
Because Noradrenaline plays a role in ADHD, it is sometimes an alternative route for medication. I took SNRIs (Selective Norprenephrine Reuptake Inhibitor) for a year hoping to avoid stimulants. It has helped but was not sufficient in my case.
Many mental health disorders are mired in myths and misconceptions — ADHD is merely one of them.