Major depressive disorder (MDD) is quite common and can be very disabling if not treated properly. However, fewer than 40% of patients achieve remission with their initial treatment. In the case of ineffective therapy, those patients often then experience months of trials using various different selective serotonin reuptake inhibitors (SSRIs), or they move on to other psychotherapists, or they drop out of treatment attempts altogether, which can be disastrous. Therefore, it would be of great importance if an objective, quantitative test were available to guide the patient towards the optimal treatment direction at the outset. Helen Mayberg and colleagues at Emory University in Atlanta have recently published an important step forward in this direction. They measured brain glucose metabolism by PET (positron emission tomography) imaging in a series of MDD patients before any form of treatment was started. They then randomly assigned the patients to either of two groups: treatment with a standard anti-depression medication (SSRI) or treatment with evidence-based psychotherapy. Of the 38 patients with clear outcomes, 12 responded well to cognitive behavioral therapy, 11 to SSRI treatment, 9 did not respond to psychotherapy, and 6 did not respond to the SSRI. They then asked whether glucose metabolism in various parts of the brain clearly corresponded to these 4 patient groups. In fact, measurement of the metabolism in the right anterior insula was able to discriminate among the groups: Lower metabolism was associated with remission in response to psychotherapy and no remission in response to SSRI treatment, while higher metabolism was associated with remission in response to SSRI treatment and no response to psychotherapy. If this finding can be reproduced in a large, prospective trial, it would mean, first, that new MDD patients could be assigned to the treatment path that is appropriate for them and with the best chance to succeed., and second, it would argue that these two groups of patients have a distinct neurophysiological basis for their MDD.
Incidentally, Mayberg has also spearheaded the use of deep brain stimulation for MDD that is resistant to any type of standard treatment. While this approach is deeply invasive, it appears to be quite promising for those patients who have run out of other treatment options.
Te observations made by Mayberg are intriguing. It is noteworthy that Suzanne Craft and others have shown that Alzheimers patients treated with intranasal insulin demonstrate improvements in activities of daily living, supposedly due to altered glucose metabolism in the brain. MDD might be another arena in which to explore the use of this novel agent. Furthermore, it raises the question: would patients with Alzheimers be candidates for this kind of testing?
Good points David. Thx, PHP
Reblogged this on asdresearchinitiative and commented:
Efficacy of treatment is the stand out point of this article.
Hi Paul
This just came across my desk so to speak , from Ohio University. It looks as though it may be important in reference to your research to bone marrow transplants (https://infectiousbehavior.wordpress.com/2012/07/17/bone-marrow-transplants-in-autism-models/ )
Hope it is of interest – http://asdresearchinitiative.wordpress.com/2013/08/22/monocytes-the-immune-system-x-neurology-anxiety/
regards
Hi Paul,
I found an interesting article called “Opinion: So depression is an inflammatory disease, but where does the inflammation come from?” (http://www.biomedcentral.com/1741-7015/11/200). Have fun reading!
Thx for the tip – that is a very interesting que and the article is worth reading. The authors suggest these factors in response to their own question: “A range of factors appear to increase the risk for the development of depression, and seem to be associated with systemic inflammation; these include psychosocial stressors, poor diet, physical inactivity, obesity, smoking, altered gut permeability, atopy, dental cares, sleep and vitamin D deficiency.” To that I would add, a deficit in resiliency to stressful events, which could come from early childhood experiences, maternal-fetal interactions, immune dysregulation (genetic & environmental) and genetic factors.
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