Joseph, on the other hand, offers a similar license to the one on my blog, so I will reproduce his post on Dopamine Abnormality in ADHD, here, with comments. To be clear, he has not offered specific permission for me to reproduce it and probably does not know that I have. He is however, kind enough to license his writing under a CC license, the details of which can be found here.
From Joseph's site;
Corpus Callosum is written by a psychiatrist at a small community hospital somewhere in midwestern USA.
A while back, Shelly wrote a nice introduction to ADHD at Retrospectacle: The Neuroscience of ADHD. Read that first, for background, then consider this to be a minor addendum. There are still people who believe that ADHD is not real. This is a good example of the scientific findings to the contrary. It is an open-access article (there is one every month) at Archives of General Psychiatry.
Depressed Dopamine Activity in Caudate and Preliminary Evidence of Limbic Involvement in Adults With Attention-Deficit/Hyperactivity Disorder
Nora D. Volkow, MD; Gene-Jack Wang, MD; Jeffrey Newcorn, MD; Frank Telang, MD; Mary V. Solanto, PhD; Joanna S. Fowler, PhD; Jean Logan, PhD; Yeming Ma, PhD; Kurt Schulz, PhD; Kith Pradhan, MS; Christopher Wong, MS; James M. Swanson, PhD
Arch Gen Psychiatry. 2007;64:932-940.
Context Attention-deficit/hyperactivity disorder (ADHD) is the most prevalent psychiatric disorder of childhood. There is considerable evidence that brain dopamine is involved in ADHD, but it is unclear whether dopamine activity is enhanced or depressed.
Objective To test the hypotheses that striatal dopamine activity is depressed in ADHD and that this contributes to symptoms of inattention.
Design Clinical (ADHD adult) and comparison (healthy control) subjects were scanned with positron emission tomography and raclopride labeled with carbon 11 (D2/D3 receptor radioligand sensitive to competition with endogenous dopamine) after placebo and after intravenous methylphenidate hydrochloride (stimulant that increases extracellular dopamine by blocking dopamine transporters). The difference in [11C]raclopride's specific binding between placebo and methylphenidate was used as marker of dopamine release. Symptoms were quantified using the Conners Adult ADHD Rating Scales.
Setting Outpatient setting.
Participants Nineteen adults with ADHD who had never received medication and 24 healthy controls.
Results With the placebo, D2/D3 receptor availability in left caudate was lower (P < .05) in subjects with ADHD than in controls. Methylphenidate induced smaller decrements in [11C]raclopride binding in left and right caudate (blunted DA increases) (P < .05) and higher scores on self-reports of "drug liking" in ADHD than in control subjects. The blunted response to methylphenidate in caudate was associated with symptoms of inattention (P < .05) and with higher self-reports of drug liking (P < .01). Exploratory analysis using statistical parametric mapping revealed that methylphenidate also decreased [11C]raclopride binding in hippocampus and amygdala and that these decrements were smaller in subjects with ADHD (P < .001). Conclusions This study reveals depressed dopamine activity in caudate and preliminary evidence in limbic regions in adults with ADHD that was associated with inattention and with enhanced reinforcing responses to intravenous methylphenidate. This suggests that dopamine dysfunction is involved with symptoms of inattention but may also contribute to substance abuse comorbidity in ADHD.
One of the key points in this study is that they did the brain scans on ADHD patients who had not been treated with drugs. One of the problems in studies like this is sometimes that it is hard to know if the abnormality was caused by the treatment, or by the condition. In order to get around that, you have to find patients who have not been treated. Then, you run the chance of biasing the results by selecting a nonrandom sample, but there is no easy way to avoid both problems simultaneously.
The study indicates that persons with ADHD have lower levels of dopamine in the emotional center of the brain (the limbic system).
I notice the last sentence in the abstract: "This suggests that dopamine dysfunction is involved with symptoms of inattention but may also contribute to substance abuse comorbidity in ADHD." I am not sure why the reference to substance abuse belongs there. It is true that there is an association between substance abuse and ADHD, but that is not the point of the study.
So there really isn't much for a laymen to add. While having ADHD certainly offers a decent perspective on the discussion, I am not a neuroscientist, nor am I anything more than a reasonably educated laymen, when it comes to psychology.
That said, Joseph's comment about the appropriateness of the comment correlating dopamine dysfunction and substance abuse, really jumped out at me. This seems like a no brainer to me, but then, I'm not a scientist. It may just be, that as this was not the stated intent of the study, it seemed an odd thing to comment on.
The thing is, that I don't think the dopamine hypothesis is a new idea. Nor is the notion that the tendency for persons with ADHD towards substance abuse being due to lower levels of dopamine very new. I mean it makes sense. The stimulant medications for ADD/ADHD stimulate the production of dopamine. Studies also seem to indicate that persons with ADHD who are medicated for it as a child, have far less a tendency for the substance abuse problems that plague many, if not most people with ADHD.
Still, it is very exciting to see more research and more studies that bring us closer and closer to understanding the physiological aspects of neurological disorders. As I have mentioned before, I see my neurological disorders as much more blessing than curse. The more we understand where they come from, how they work, the better we'll be able to deal with the harshest aspects of them, while maintaining the most positive aspects of neurodiversity.