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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 4 of 4. This is the beginning of the thread.
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?
Posted by zeugma on May 12, 2004, at 21:15:18
In reply to query for psychopharmocologists, posted by zeugma on May 12, 2004, at 19:20:57
Behav Brain Res. 1989 Aug 1;34(1-2):117-30. Related Articles, Links
Increased waking as well as increased synchronization following administration of selective 5-HT uptake inhibitors to rats.Ursin R, Bjorvatn B, Sommerfelt L, Underland G.
Department of Physiology, University of Bergen, Norway.
Sleep and waking stages and EEG power spectra were investigated in rats following saline injections and injection of 10 and 20 mg/kg zimeldine or 10 and 20 mg/kg alaproclate, both selective 5-HT reuptake inhibitors. Following zimeldine there was a biphasic effect on sleep and waking, waking being increased during the first 2 1/2 h of recording, while slow wave sleep (SWS), in particular highly synchronized SWS-2 with high slow wave activity, was increased during the second 2 1/2 h recording period. Analysis of EEG power spectra indicated that the amount of synchronized slow wave activity was also increased within the sleep that occurred during the waking-dominated initial 2 1/2 h period. These data suggest simultaneous appearance of increased waking and increased synchronization following general serotonergic stimulation. They are interpreted as due to effects on different regions of the serotonergic system or on different serotonergic receptors. Consistent with earlier findings, zimeldine also suppressed rapid eye movement (REM) sleep. Following alaproclate, a clear waking effect was present, but only a weak synchronizing effect was seen. This is consistent with data on regional differences in uptake inhibition for zimeldine and alaproclate. Alaproclate also reduced REM sleep. Zimeldine or alaproclate was also administered to rats that had reduced sleep following pretreatment with a moderate dose of parachlorophenylalanine (PCPA). None of the drugs increased waking any further, but the PCPA-pretreated animals that received zimeldine had increased SWS-2, indicating that the SWS-2 increase following zimeldine alone was not a rebound effect.
Posted by King Vultan on May 14, 2004, at 16:43:26
In reply to query for psychopharmocologists, posted by zeugma on May 12, 2004, at 19:20:57
I looked into the effects of Strattera vs. other selective norepinephrine reuptake inhibitors last year when I tried several of these. My conclusion after looking at various studies was that the tricyclics that are selective for NE reuptake (nortriptyline, desipramine, protriptyline) are similar to Strattera in their ancillary effects on dopamine.
As to which is the best for ADD, well, YMMV, but I thought Strattera was perhaps somewhat more stimulant-like than the others (this is a admittedly a guess on my part, as I have never actually tried a stimulant). It seemed to me that Strattera had more of a powerful, sledgehammer effect, and the tricyclic most similar to it, which is desipramine, had a gentler, more easy going nature. Keep in mind, though, that the basic nature of their therapeutic effect was more or less the same; the difference seemed to be in the manner and rate at which the effect was delivered.
Todd
Posted by zeugma on May 15, 2004, at 12:00:51
In reply to Re: query for psychopharmocologists, posted by King Vultan on May 14, 2004, at 16:43:26
Interesting. I was able to find absolutely nothing regarding a differential effect of Strattera on the dopamine system in comparison to the tricyclics. The only thing I turned up (and it's very dubious, since the dose the elicited the highest response in rats is approximately eight times the dose I use) is that Strattera, unlike other NE reuptake inhibitors, blocks K+ channels. This boosts the levels of all the amines, and has an antidepressant-like effect in behavioral tests.
For what it's worth, Strattera does seem to have a much more specifically 'alerting' effect than nortriptyline. But this could simply be a combination of much faster absorption rate (nortriptyline takes 8 hrs. to reach peak plasma levels, while Strattera takes an hour or less), lack of H-1 sedation, and greater affinity for the NE transporter itself. While I can't dismiss my pdoc's claim, what you say doesn't corroborate it either. So I will keep looking, and will have more questions for my pdoc at next visit.
Meanwhile, reducing nortriptyline to 50 mg has resulted in a lessening of fatigue, allowing me to begin a mild exercise regimen, which is starting to lift my mood. At the same time, increasing Klonopin to .5 mg bid is causing less of the late-afternoon/evening 'meltdowns' that were depressing, to say the least, and made me fear that I would lose my job, since these meltdowns would always occur in the presence of my colleagues.
This is the end of the thread.
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