PrintNeuroscience 101, Part 2
Neurotransmitter deficiencies
Brain scientists have found that deficiencies in specific neurotransmitters underlie many common disorders, including anxiety, depression, anger-control problems, and obsessive-compulsive disorder.
ADHD was the first disorder found to be the result of a deficiency of a specific neurotransmitter — in this case, norepinephrine — and the first disorder found to respond to medications to correct this underlying deficiency. Like all neurotransmitters, norepinephrine is synthesized within the brain. The basic building block of each norepinephrine molecule is dopa; this tiny molecule is converted into dopamine, which, in turn, is converted into norepinephrine.
A four-way partnership
ADHD seems to involve impaired neurotransmitter activity in four functional regions of the brain:
- Frontal cortex. This region orchestrates high-level functioning: maintaining attention, organization, and executive function. A deficiency of norepinephrine within this brain region might cause inattention, problems with organization, and/or impaired executive functioning.
- Limbic system. This region, located deeper in the brain, regulates our emotions. A deficiency in this region might result in restlessness, inattention, or emotional volatility.
- Basal ganglia. These neural circuits regulate communication within the brain. Information from all regions of the brain enters the basal ganglia, and is then relayed to the correct sites in the brain. A deficiency in the basal ganglia can cause information to “short-circuit,” resulting in inattention or impulsivity.
- Reticular activating system. This is the major relay system among the many pathways that enter and leave the brain. A deficiency in the RAS can cause inattention, impulsivity, or hyperactivity.
These four regions interact with one another, so a deficiency in one region may cause a problem in one or more of the other regions. ADHD may be the result of problems in one or more of these regions.
Trial and error
We don't know which brain region is the source of ADHD symptoms. Nor can we tell whether the problem lies with a deficiency of norepinephrine itself or of its chemical constituents, dopa and dopamine. Thus, doctors must rely on clinical experience to determine which medication to try for each child, and at what dosage.
Someday, when our knowledge of the brain is greater, the diagnosis and treatment of ADHD will be more nuanced. Instead of diagnosing simply "ADHD," and prescribing a stimulant, we might be able to say, "Billy's ADHD is caused by a deficiency of dopa in the frontal cortex, so he needs medication A," or "Mary has a type of ADHD caused by a deficiency of dopamine in the limbic system, so she needs medication B," or "José has ADHD caused by a deficiency of norepinephrine in the reticular activating system, and he needs medication C."
What do ADHD medications do? In simple terms, they raise the level of norepinephrine within the brain. (Stimulants work by causing the brain to synthesize more norepinephrine; nonstimulants by slowing the rate at which norepinephrine is broken down.) Once the level is where it should be, the brain functions normally, and the individual becomes less hyperactive, inattentive, and/or impulsive. Once the drug wears off, the level falls — and symptoms return.
And so we come to the conclusion of Neuroscience 101. I hope you have a greater knowledge of, and appreciation for, the human brain. I also hope you have a better understanding of neurotransmitters and how they are linked to ADHD.
In years to come, I'm sure we will gain a more comprehensive understanding of ADHD — and new medications that will be more effective than those we have now. I can't wait.
This article comes from the December 2006/January 2007 issue of ADDitude.
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