Posted by zeugma on May 12, 2004, at 19:20:57
So after last Friday's lengthy meeting with pdoc, I made some changes. The nortriptyline was reduced from 75 to 50 mg. The clonazepam was upped (yesterday) from .75 mg/day (.5 mg am/.25 mg pm) to .5 mg bid. I have a Lexapro starter pack (10 mg capsules) so that can be my next move, if I want, or I can try clomipramine instead.
I asked him some questions about the TCA/Strattera combination (I take 80 mg Strattera am). He claimed that the secondary amine TCA's nortriptyline and desipramine work more in the brainstem, while Strattera works more on the frontal lobes. I obviously can't determine by introspection where the molecules are going in my brain, and I have been unable to uncover anything online remotely suggesting this, which of course doesn't mean that he is wrong in what he says. there is in fact a literature, dating back to the late 1970's and early 80's, dealing with the differences in effects on sleep studies conducted on animals of various early SSRI's (zimelidine and alpracate (sp.)) observed and attributed to differential locations of effect on regions innervated by the serotonin transporter. Does ANYONE know anything about this kind of research? I thought, if I read the study on atomoxetine conducted by Eli Lilly scientists properly, that atomoxetine, reboxetine, and desipramine had essentially similar effects on the norepinephrine transporter and its interactions with the dopamine system in the prefrontal cortex. My pdoc claims this isn't so, and furthermore, that atomoxetine is superior to desipramine in the treatment of ADD. can anyone shed light on this matter?
poster:zeugma
thread:346261
URL: http://www.dr-bob.org/babble/20040510/msgs/346261.html