During emergency medicine residency, all of us were “pimped” regularly on the toxidrome du jour. Each attending had their favorite, and by the end of training, you could predict which answer to blurt out before they even started the question. We had the intoxication syndromes, the withdrawal syndromes, the encephalopathies, the psychoses, etc. However, the word “addiction” was never associated with the explanations given for any toxidromes.
Addiction is a chronic neurobiological disorder that causes a derangement of the reward system, creating characteristic behaviors that stem from the drug replacing all other natural rewards. In fact, the behaviors are so characteristic that they are how the DSM-5 diagnoses the disease. Yet, we tend to perceive these behaviors in our emergency departments as frustrations rather than symptoms of the disease that is the number-one cause of injury-related death in our country.
What drives these behaviors? All addictions have a final common pathway that causes a decrease in the dopamine produced in the nucleus accumbens (NAc) and the ventral tegmental area (VTA). This decrease in dopamine leads to a baseline anhedonia (flat affect with lack of inherent motivation) that is, in the patient’s mind, only reversed with their drug of choice. When a patient says that they are using so that they can feel “normal,” this matches the neurobiological truth.
So how does this happen? We’re glad you asked!
Biology of Addiction
Generally, our reward center produces a stable amount of dopamine on a daily basis that lets us get out of bed, migrate to the coffee maker, and, despite the inner voice begging for the beach, go to work. With a natural stimulus like winning the lottery (or the scheduler forgetting to put you on the holiday schedule), we produce about 100 ng/dL of dopamine in the reward system. On the worst day—you know, the day you pull the backup call ripcord—our NAc produces about 40 ng/dL. This is the “normal” range of dopamine (aka motivation).
When a patient (or one of us) uses an addictive substance, dopamine goes up 10 times higher than the normal range. As with other systems in the body, the brain fights back with aggressive movement toward homeostasis. It decreases the amount of dopamine released. If the patient continues to use, then the body decreases the amount of dopamine produced, which then atrophies the neurons. Finally, with continued use, the brain may kill the dopamine-producing neurons via apoptosis. This neurobiology may make you think back to college and wonder if you could blame alcohol and subsequent low dopamine for lack of motivation to finish charts. So far, we’ve found that compliance officers are not buying it. Hopefully, this is starting to explain why addiction is much more complicated than, “The patient is just making poor decisions,” and you better understand why telling them, “You could have died!” is generally ineffective. Additionally, it explains why attempting basic reasoning with the patient doesn’t work and just frustrates you, and the patient, further.