Posted by paulk on June 28, 2001, at 5:11:25
In reply to MAOIs, benzos, etc. » paulk, posted by Elizabeth on June 27, 2001, at 10:31:20
> > The Nardil has just kicked in the last week or so I still question that the low BP is caused by other than the increase in the monoamines from what I understood until 90% of the MAO is knocked out There isnt enough rise in neuro transmitters to do anything.>No, the increase in neurotransmitter concentrations takes place immediately.
This is not at all what my doctor told me??? He said that the reason they ramp the drug up to 60mg/day is that it takes some time to knock out enough MAO to effect the monoamines after that, the MAO level can be kept low by a lower dosage that is only knocking out the amount that the body is replacing.
>That's not directly responsible for the antidepressant effect of the drug, but a lot of the side effects, direct or indirect, happen sooner, orthostatic hypotension being one of these. MAOIs (and tricyclics) decrease the compensatory cardiovascular response to changes in posture.
Im going to have to check into this I always want to understand how a drug is working you have raised some doubts about the model I had in my head (of what the drugs were doing in the same place.< grin >)
> > I seem to be doing OK except I am starting to have trouble with word selection and sometimes the wrong word will come out.
>That's a common effect of antidepressants, especially tricyclics and MAOIs. Anticholinergic drugs are the worst that way, but norepinephrine has some effects that oppose those of acetylcholine. MAOIs upset the reciprocal interaction between NE and ACh; as a result, they virtually abolish REM sleep. In light of this, their effects on implicit or associative memory are surprisingly subtle.
Hmmm I have had the same effect on higher dosages of Effexor 150mg/day
> I wonder if it is a side effect of the GABA?
In the case of Nardil, that might have something to do with it too. (I had the word-finding problems on Parnate as well, although it wasn't a big deal with any of the MAOIs.)> >Perhaps I should take the med at night?
>I tried taking Nardil on every imaginable dosing schedule. Didn't make any difference in any of the side effects.
Thats what my doctor said also.
> > I am still at the high dose 60/mg day perhaps it will get better when they lower the dosess back down.
>I don't think that's such a good idea. First of all, 60 mg is *not* a "high" dose; it's a normal dose. Also, although it was once thought that the right way to give people antidepressants was to start with a high "loading" dose and then decrease it down to a very low "maintenance" dose, this has proven not to work very well.
Ive only seen this dosing scheme suggested for Nardil?? If the idea is to bring down the level of MAO and then maintain it there; it makes sense. That is the pills knock out so much MAO enzyme after which you just need to knock out what the body replaces thus a lower dose. Im going to have to dig into this deeper.
> (My own experience with MAOIs bears this out: at one point I tried decreasing the Nardil to 30 mg, and my depression and panic started coming back.
Now, if the drug has a dual MAO plus a GABA effect. I could see that the MAO level could be maintained at a low dose, but to maintain a higher level of GABA might require a higher dose, which would explain return of panic attacks. (Thats a lot of ifs, but I dont remember seeing that the increase in GABA was due to the missing MAO so I could imagine that it could have a different dose dependency than the increase in Monoamines.)
> > Was the inhibition of the GABA metabolism a direct effect of the drug or secondary?
>I'm still not sure what you mean by that (although I know what *I* would mean < g >). I'm also not sure the mechanism is known. But I believe it's an early effect, not one that takes a week or more to happen.
OK, a primary effect of a MAOI would be the knocking out of the MAOI the secondary effect would be a resulting increase of mon-amine transmitters (Seritonin, Dopamine, Ne) due to the missing MAO.
Another example a SSRI has a primary effect blocking the reuptake the secondary effect would be the increase in seritonin level, a terserary effect could be a resulting promotion of new neuron generation, a fourth level effect would be improved memory function. Each of these effects has a different time frame associated with it.
My hunch, which could easily be wrong, but I hope to find the answers, is that the lowBP is not caused by the increase in Monoamines, but is a different effect of the drug. And I wonder if the same is true for the GABA effects of Nardil.
On to the benzos....> > He was taking I think it was Restaril (sp??) . He was very bi-polar yet a dear friend very smart didnt usually go psychotic in his mania. He really needed to be in a halfway house to have someone monitor is medications. The lack of supervision is what I blame for his death. I think the benzos may have surpressed his gag reflex or dis-coordinated his swallowing enough to cause the problem.
It was my understanding that he had been using only benzos for the last 5 years.>Restoril (temazepam) is generally prescribed only for insomnia, not for daytime anxiety. It is unlikely that your friend was prescribed this medication in very large doses.
He may have been getting them from 2 or three doctors at once. Probably not the best medicine for a Biopolar but he seemed to enjoy his manias might have just wanted to be able to sleep and return to his mania the next day.
> Most of these people were in the hospital because they had benzo problems sort of self-selected. Remember everyone reacts differently.
> > I would take it for anxiety and it worked wonderfully but then as it wore off I would feel even worse than before.
>I guess I'm confused. What sort of anxiety were you taking it for? (Any diagnosis?)
GAD with mixed depression probably better called atypical depression in my case.
> > I would say that irritability is a symptom of anxiety??
>I guess it depends on your definition. I usually think of anxiety as involving inhibition, and irritability as involving disinhibition.
I define anxiety as fear/worry some people try to control fear by avoiding the stimulus, others by fighting it (sounds like fight / flight adrenalin). I have done a bit of both getting irritable /angry has the advantage of giving the illusion of being in control. At times I have had panic attacks light headed, heart palpitations, shaky hands and voice. But I can go long times with out those symptoms and will get quite irritable if I feel Im getting pushed into a situation that will cause me anxiety.
I wonder if depression is an adaptation to anxiety hypersomnia, not eating, less active, fatigue, low self estemem would all help a cave man avoid anxiety producing situations.
>Did this "rebound anxiety" happen the very first time you took Xanax? And how often were you taking it? (Frequent use, even if it's not around-the-clock, can lead to some degree of dependence.)First time half pill in the morning that evening I had rebound anxiety and even edgy the next day.
Paulk
poster:paulk
thread:65795
URL: http://www.dr-bob.org/babble/20010625/msgs/68207.html