Posted by SLS on March 2, 2002, at 8:46:10
In reply to Re: When is duloxetine to be approved? » SLS, posted by JohnX2 on March 1, 2002, at 19:03:13
Hi John.
Hi Medlib.
> So what's the status of your Effexor trial? You didn't sound
too upbeat in your earlier post. :(Things got to be a mess. I'm pretty sure that Effexor provided some positive effects early on. As I reported them to my doctor, they were significant enough to justify its continuation. Unfortunately, nortriptyline, the tricyclic I chose to add, proved to be confounding. When it exerts an antidepressant effect, the quality of the improvement it produces is the best of the tricyclics I have yet tried (imipramine, desipramine, amitriptyline, nortriptyline, protriptyline, and amoxapine). However, this improvement has been episodic and transient (1/2 to 2 days), and always follows a dosage change, either up or down. It seems that no therapeutic window exists for me. My doctor told me that this situation occurs in as many as twenty percent of people for whom nortriptyline provides some relief. I find that figure extremely large, but I do qualify. Even so, for some reason, he decided to continue with it for over seven months. In retrospect, this was obviously too long. I fault both my doctor and myself for this.
What I decided to do was to ask to switch from nortripyline to imipramine, a drug that has demonstrated a very predictable behavior for me. While still taking 300mg of Effexor, I experienced an extreme worsening of my depression after less than a week of the switch. I couldn't help but to blamed Effexor for this, and decided to discontinue it as it seemed now to be hurting more than helping. Getting off of it was very easy. I have come to discontinue some medications by making dosing "on-the-fly". Although I follow a general schedule of dosage reduction, I simply wait until I begin to feel the onset of withdrawal effects, and dose accordingly. I either nibble off a piece of the original immediate-release tablet or "eyeball" an amount of the pellets of the XR preparation contained within a capsule. I pretty much determine the amount of either by "feel", and judge this according to how I reacted to the previous dosing. Anyway, it worked well enough to get off of 300mg of Effexor within a week's time. One must take into consideration that I remained on a tricyclic throughout this period, and that the NE reuptake inhibition it continued to produce mitigated some of the withdrawal effects from discontinuing Effexor. Regardless, I have used this method successfully with Paxil and various benzodiazepines.
After discontinuing Effexor and experiencing a welcome return of drive and motivation (along with a vocabulary), I decided to revisit nortriptyline. Indeed, there is no single dosage that produces a stable improvement. 75mg is too little and 100mg is too much. Both dosages put my blood-levels within the 50 - 150 therapeutic range. I switched back to imipramine yesterday. At this point, I must entertain the idea of reintroducing Effexor to be sure that I don't mistakenly overlook a successful treatment (Lamictal 300mg; imipramine 200mg - 300mg; Effexor 300mg - 450mg. Perhaps nortriptyline left my system altered in a way that allowed imipramine to produce this effect. I should probably wait to first establish the optimum dosage of imipramine. However, I don't know if I have the patience to do so. I was hoping that duloxetine would be approved very soon so that I could explore it before returning to Effexor or switching to Nardil.
> Btw, have you been reevaluated as a DST
non-suppressor?I am a DST non-suppressor according to tests taken over ten years ago. I don't know of any reason to believe that the older tests were invalid, but I guess it is possible.
> I'm curious what the current thinking is of
your treating physicians? I.E. what rationale
do they have for going direction A vs. direction B ?
Just wondering.Me too.
I think I'll stick with him a while longer - probably through a trial of Nardil. I need to see what cards he's holding in his hand that I haven't seen yet. Perhaps he is not as aggressive and creative to treat someone like me as I was led to believe.
> I was reading an interesting article in
regards to treatment resistant mood disorders
thinking in terms of my own poop out syndrome:
http://www.acnp.org/g4/GN401000110/Default.htm
It suggested using a calcium channel blocker
such as nimodipine. This blocks calcium flux
through NMDA channels. An nmda antagonist like
memantine would work as well I believe.I'll see if I can get through the article. What are its salient points, and how do you interpret them? I'm good for about four or five sentences before my brain gives out. It might take a long time to get through. Here's one for you: I find that if I push myself to read beyond a few paragraphs, my depressed state worsens - not only immediately afterwards, but for the rest of the day. It actually feels as if I completely empty an already empty tank of gas. I always feel guilty for writing posts as long as this one because I know that I wouldn't be able to get through it if I had to read it myself.
> Sorry I'm so nosy.
I'm glad you are, although I perhaps replace the word "nosy" with "concerned". I like to think so, anyway.
> I'm just curious what the current
indicators are as to why your medicines would not be
kicking in (I'm sure you got me beat on this one).I'm not sure I understand the question.
I am still searching for an adequate term to use in place of the word "depression" to be able to accuately portray the nature of affecive disorder as I and many others experience it. As I see it, I suffer from a brain disorder that outwardly and superficially resembles what an otherwise healthy person experiences when they get depressed about something.
> Best Wishes Always,
JohnBack at 'ya.
Oh yeah, I am becoming interested in aripiprazole (Abilitat) as a potential adjunct to antidepressants.
http://www.medscape.com/viewarticle/422878
I have experience a small, but significant when I have added the following atypical APs to antidepressants: olanzapine, risperidone, and ziprasidone. Unfortunately, when I arrive at a dosage that produces an optimal improvement, I also experience unacceptable cognitive side-effects. Dr. Smith believes that this is being caused by DA receptor antagonism rather than antagonism at the 5-TH2 receptor. Hopefully, aripiprazole will not cause these effects because it is a "partial" agonist of DA (dopamine) receptors.
<excerped from the article appearing at Mescape>"Stephen M. Stahl, M.D., Ph.D., Professor of Psychiatry at the
University of California at San Diego, places aripiprazole in the
class of antipsychotics called dopamine system stabilizers (DSSs).
Stahl dubs these new therapeutic agents "Goldilocks" because of
their ability to strike a balance between too much and too little
dopamine. [Editor's Note: The common pharmacologic terminology for
aripiprazole would be a partial dopamine agonist in contrast to
other antipsychotic drugs that are dopamine antagonists. -- SRS]"
- Scott
poster:SLS
thread:95939
URL: http://www.dr-bob.org/babble/20020301/msgs/96054.html