Creating a free account will enable you to subscribe to our daily and weekly email newsletters, as well as customize your reading experience to show only the categories most relevant to you.
Signing up only take a few minutes, so why not give it a try and see what you've been missing out on.
A new study by the University of Cambridge in the UK questions the widely held view that dysfunction in dopamine - a chemical that controls the brain's reward and pleasure centers - is the main cause of ADHD, a condition characterized by inattentiveness, hyperactivity and impulsiveness.
Writing in the latest issue of the journal Brain, the researchers, from the University's Medical Research Council (MRC)/Wellcome Trust Behavioural and Clinical Neuroscience Institute (BCNI), suggest instead that the main cause of attention deficit hyperactivity disorder (ADHD) is to be found in structural differences in the brain's grey matter.
They hope their findings will significantly improve our understanding of the cause of ADHD and help improve future treatments.
Dopamine is a chemical naturally produced in the brain that is important for concentration or sustained attention, working memory and motivation. It helps carry signals between brain cells by attaching to dopamine cell receptors - special entry-points in cell membranes that can only be opened by that particular molecule.
Ritalin - a drug approved for the treatment of ADHD - works by raising levels of dopamine, causing more to bind to the cells and thus increase the communication between them.
In their landmark study, the researchers used a combination of positron emission tomography (PET) and magnetic resonance imaging (MRI) to measure grey matter and dopamine receptors and determine how the drug methylphenidate (Ritalin) affected dopamine in patients with ADHD and healthy people without the condition.
Both groups of participants were given either a dose of Ritalin or a placebo. The study was double-blinded, which means neither the participants nor the clinicians who administered the medication knew whether they were using Ritalin or the placebo.
Before and after taking their given dose, participants completed tasks that tested their ability to concentrate and pay attention over a period of time.
The team found that both the ADHD patients and the controls who were given Ritalin showed similar increases of dopamine in their brain. They also showed equivalent levels of improvement in the attention and concentration tasks.
The researchers also found that although participants with ADHD as a group had significantly less grey matter in the brain, and performed much worse in the attention tests than the healthy controls, they had similar levels of dopamine receptors in an area of the brain called the striatum, and Ritalin increased dopamine in this area to the same degree.
This important finding suggests there was no underlying dysfunction in dopamine per se.
The researchers were interested to see that Ritalin also increased sustained performance in some of the healthy controls, suggesting the overall ability of the drug to increase attention performance in both ADHD and control participants was related to the rise in dopamine it caused in the striatum.
Study leader Prof. Barbara Sahakian says the results are important because they show Ritalin improves attention and concentration regardless of whether people have ADHD or not:
"These new findings demonstrate that poor performers, including healthy volunteers, were helped by the treatment, and this improvement was related to increases in dopamine in the brain."
Co-author Professor Trevor Robbins, Director of the BCNI, says:
"These findings question the previously accepted view that major abnormalities in dopamine function are the main cause of ADHD in adult patients. While the results show that Ritalin has a 'therapeutic' effect to improve performance, it does not appear to be related to fundamental underlying impairments in the dopamine system in ADHD."
The study was funded by the MRC.
According to a study published in the Journal of the American Academy of Child and Adolescent Psychiatry in 2011, children's ADHD drug response depends on variants in specific dopamine genes.
Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without the permission of Medical News Today.
A positron emission tomography study of nigro-striatal dopaminergic mechanisms underlying attention: implications for ADHD and its treatment; Natalia del Campo, Tim D. Fryer, Young T. Hong, Rob Smith, Laurent Brichard, Julio Acosta-Cabronero, and others; Brain Volume 136 Issue 11 November 2013, 3252-3270; DOI: 10.1093/brain/awt263.
Additional source: University of Cambridge news release 28 October 2013.
Visit our ADHD category page for the latest news on this subject.
Please use one of the following formats to cite this article in your essay, paper or report:
Paddock, Catharine. "ADHD cause unlikely to be dopamine dysfunction." Medical News Today. MediLexicon, Intl., 29 Oct. 2013. Web.
13 Dec. 2013. <http://www.medicalnewstoday.com/articles/268016>
Paddock, C. (2013, October 29). "ADHD cause unlikely to be dopamine dysfunction." Medical News Today. Retrieved from
Please note: If no author information is provided, the source is cited instead.
If you write about specific medications, operations, or procedures please do not name healthcare professionals by name.
For any corrections of factual information, or to contact the our editorial team, please use our feedback form. Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
This page was printed from: http://www.medicalnewstoday.com/articles/268016.php
Visit www.medicalnewstoday.com for medical news and health news headlines posted throughout the day, every day.
© 2004-2013 All rights reserved. MNT (logo) is the registered trade mark of MediLexicon International Limited.