Posted by Larry Hoover on April 24, 2003, at 10:41:18
In reply to Re: Larry..Question I've been wondering for long time » Larry Hoover, posted by pelorojo on April 23, 2003, at 15:03:00
> > In my thinking, psychotropic meds are more like the high-octane boost or the heavy oil. They mask the problem, and do nothing to remedy the underlying difficulties. Moreover, it would always be a mistake to expect the car to run "as new".
> >
> Is that true ("do nothing to remedy the underlying difficulties")? I thought there was speculation that anti-depressants (SSRIs, at least) stimulate neurogenesis in some strategic parts of the brain and that was part of how they worked. If true, it seems that in some way it would get at the underlying problem -- no ?Yes, when they work. I don't mean to sound defensive, but it's reasonable to assume that there are always conditions under which a statement is true, and others where it is not. My choice of language does suggest an absolute, and I didn't really mean it that way....
So, I'll expand on this a little bit. Recent functional neuroimaging studies have shown that there are trends towards the restoration of normal metabolic levels in different regions of the brain when antidepressant treatment is associated with remission of symptoms, but some regions of abnormal metabolic functioning are not restored to normalcy. The reasonable conclusion is that antidepressant therapy is an incomplete treatment for depression; the underlying pathology continues, even in remission. This failure to treat whatever else is still wrong may be related to the phenomenon of med poop-out (my speculation).
Neil Young said that "rust never sleeps". I think he was right.
Lar
Eur Neuropsychopharmacol 2002 Dec;12(6):527-44Functional 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, USANeurophysiological 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.
poster:Larry Hoover
thread:221042
URL: http://www.dr-bob.org/babble/20030423/msgs/221978.html