Posted by Larry Hoover on May 29, 2007, at 17:40:43
In reply to Brain scans and antidepressants, posted by Denise190466 on May 27, 2007, at 14:56:53
> Are scientists yet able to see from brain scans what is happening to the brain when somebody responds positively to an antidepressant compared to when they don't respond well? i.e what is happening to receptors and in what parts of the brain.
>
> I'd love to know why my brain used to respond so well to them and yet now doesn't.
>
> DeniseThere are a number of studies which show metabolic abnormalities in depressed, and in depressed-but-in-remission brains. They can see changes that occur in response to treatment. Somewhat similar changes occur in both drug-treated subjects and those receiving cognitive-behavioural therapy....if the treatment is successful. Non-responders tend to continue to resemble untreated depressed subjects' brains.
The studies I'm referring to demonstrate regional brain activity, by measuring glucose consumption. The resulting image, a PET scan, shows brighter regions where glucose metabolism is high. In depressed brains, some regions that would be active in a healthy brain are not active, whereas other regions are much more active when compared to healthy subjects. Successful treatments do normalize some of these disturbances, but others remain abnormal.
The take home message is that antidepressant treatment is, at best, an incomplete treatment for depression. Same goes for therapy. Whatever the pathophysiology of depression really is, it likely continues to change the brain, despite treatment.
Here are some references....
The first one is pretty much right on the subject you enquired about, IMHO. Immediately below the abstract is a link to the full-text, for those interested. Next, below that, is a nice summary of the various theories of depression (excellent graphics). The last two are a couple of full-text imaging studies. They're quite large .pdf files, because they contain images.
Lar
Eur Neuropsychopharmacol. 2002 Dec;12(6):527-44.
Functional anatomical correlates of antidepressant drug treatment assessed using PET measures of regional glucose metabolism.
Drevets WC, Bogers W, Raichle ME.
Neuroimaging in Mood and Anxiety Disorders Section, National Institutes of Health, NIMH/MIB, Bethesda, MD 20892, USA. drevetsw@intra.nih.govNeurophysiological studies of major depression performed using PET imaging have shown abnormalities of regional cerebral blood flow (CBF) and glucose metabolism in multiple prefrontal cortical and limbic structures that have been more generally implicated in emotional processing. The current study investigated the effects of antidepressant drug treatment in these regions using PET measures of glucose metabolism. Subjects with primary MDD (n=27) were imaged while unmedicated and depressed, and, of these, 20 were rescanned following chronic antidepressant drug treatment. Regional metabolism was compared between unmedicated depressives and controls and between the pre- and post-treatment conditions in regions-of-interest (ROI) where metabolism or flow had previously been shown to be abnormal in unmedicated depressives. At baseline, the mean metabolism was increased in the left and right lateral orbital cortex/ventrolateral prefrontal cortex (PFC), left amygdala, and posterior cingulate cortex, and decreased in the subgenual ACC and dorsal medial/dorsal anterolateral PFC in the unmedicated depressives relative to controls, consistent with the results of previous studies. Following treatment, metabolism significantly decreased in the left amygdala and left subgenual ACC, and corresponding changes in the orbital and posterior cingulate cortices approached significance. The metabolic reduction in the amygdala and right subgenual ACC appeared largely limited to those subjects who both responded to treatment and remained well at 6 months follow-up, in whom the reduction in amygdala metabolism tightly correlated with the reduction in HDRS scores. The magnitude of the treatment-associated, metabolic change in the amygdala also correlated positively with the change in the stressed plasma cortisol levels measured during scanning. These data converge with those from other PET studies to indicate that primary MDD is associated with abnormal metabolism in limbic and paralimbic structures of the mesiotemporal and prefrontal cortices. Chronic antidepressant drug treatment reduces metabolism in the amygdala and ventral ACC in subjects showing a persistent, positive treatment response. In contrast, the persistence of the abnormal metabolic deficits in the dorsomedial/dorsal anterolateral PFC in MDD during treatment may conceivably relate to the histopathological changes reported in these regions in post mortem studies of MDD.
http://www.nature.com/nrn/journal/v6/n3/full/nrn1629.html
poster:Larry Hoover
thread:759825
URL: http://www.dr-bob.org/babble/20070524/msgs/760233.html