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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 9 of 9. This is the beginning of the thread.
Posted by AMenz on July 5, 2001, at 17:55:07
I had been progressing nicely and doctor prescribed Buspar (I'm also on Zoloft, Carbomepazine, Lorezapam).
I've now been taking it for two weeks and feel serious symptoms, agitated, racing thoughts, volatility. This is getting so severe it's affecting family situation.
Please help anyone who can confirm if they have this kind of experience.
Posted by Elizabeth on July 6, 2001, at 1:26:44
In reply to Going Crazy: Could it be Buspar????? , posted by AMenz on July 5, 2001, at 17:55:07
> I had been progressing nicely and doctor prescribed Buspar (I'm also on Zoloft, Carbamapezine, Lorazepam).
>
> I've now been taking it for two weeks and feel serious symptoms, agitated, racing thoughts, volatility. This is getting so severe it's affecting family situation.It sounds like you might be having a manic reaction due to the combination of antidepressants (BuSpar, despite being marketed for anxiety, is basically an antidepressant and has been known to trigger mania). Call your pdoc (page him/her if possible), and let your family know that you're having a drug reaction (if you're comfortable talking to them about it, of course).
-elizabeth
Posted by Mitch on July 7, 2001, at 10:28:25
In reply to Going Crazy: Could it be Buspar????? , posted by AMenz on July 5, 2001, at 17:55:07
AMenz,
YES, BUSPAR CAN CAUSE THAT. That is precisely what happened to me when I was taking 10mg/day! The interesting thing is that I lost all fear of neary everything (GAD-social anxiety). Instead of being afraid of people I was ready to kick their ass all the time! I had some really bad shouting matches at work and almost got fired!
I do know that it *reduces* serotonin and Zoloft which calms my temper increases serotonin. I dx'd it and within a couple of days the hostility stopped! I don't *think* it is the dopamine receptors it affects-because I can take a dopamine agonist and it just makes me sleepy. It has got to be the 5-HT1a agonist activity it has-that triggers the hostility.
Mitch
> I had been progressing nicely and doctor prescribed Buspar (I'm also on Zoloft, Carbomepazine, Lorezapam).
>
> I've now been taking it for two weeks and feel serious symptoms, agitated, racing thoughts, volatility. This is getting so severe it's affecting family situation.
>
> Please help anyone who can confirm if they have this kind of experience.
Posted by Elizabeth on July 8, 2001, at 15:35:57
In reply to Re: Going Crazy: Could it be Buspar????? » AMenz, posted by Mitch on July 7, 2001, at 10:28:25
> I do know that it *reduces* serotonin and Zoloft which calms my temper increases serotonin.
?
Buspar imitates the action of serotonin at a particular site (the 5-HT1a receptor, believed to be involved in depression and some types of anxiety) -- it's what's called a partial agonist at this receptor. That doesn't mean it "reduces" serotonin.
If it was making your temper or mood worse to a point where you couldn't function, then it probably was best to go off it (without any need to speculate about the mechanism whereby it did this). What dose were you taking, and for how long?
-elizabeth
Posted by Mitch on July 8, 2001, at 16:45:45
In reply to Re: Going Crazy: Could it be Buspar????? » Mitch, posted by Elizabeth on July 8, 2001, at 15:35:57
Elizabeth-trust me I wasn't speculating about mechanisms when I stopped it! It was after I stopped it and the hostility subsided that I began to speculate-because I liked the effect it had of nearly completely eliminating almost all of my anxiety-that is a mind-blowing feat in itself-that is what got my curiousity about mechanisms. I was taking 5mg/day for about two weeks-felt much lowered anxiety, but I was starting to gripe and complain about stuff at work more often. Then I boosted it to 10mg/day for about another week, that was when the hostility kicked in. I would get so angry my heart would just race and race, and I would be thinking all sorts of hostile stuff "That asshole is going to get some payback you'll see!"-and worse than that. I slept ok-I wasn't euphoric or agitated (not classicly hypomanic). It was like I LIKED BEING PISSED OFF-so it wasn't any kind of miserable dysphoria in that sense.
I am not that interested in *how Buspar works* so much as *why did I get so hostile when I took it*.
When I mentioned the *lowered serotoinin* I was referring to what the patient sample package described. It said that excessive anxiety could be due to an excess of serotonin and that Buspar worked to reduce excessive serotonin-or something to that effect. Then when I was checking out the drug itself I came across this medline abstract-that made it appear that extracellular serotonin was being cut, while extracellular DA and NE was getting boosted. The extracellular DA is probably what caused my hostility, but not sure.
Anyhow, here goes;Neuroscience 1999;93(4):1251-62
Buspirone modulates basal and fluoxetine-stimulated dialysate levels of dopamine, noradrenaline and serotonin in the frontal cortex of freely moving rats: activation of serotonin1A receptors and blockade of alpha2-adrenergic receptors underlie its actions.
Gobert A, Rivet JM, Cistarelli L, Melon C, Millan MJ.
Institut de Recherches Servier, Psychopharmacology Department, Croissy-sur-Seine, Paris, France.
The serotonin1A receptor partial agonist, buspirone, also displays antagonist properties at D2 receptors and is metabolized to the alpha2-adrenergic receptor antagonist, 1-(2-pyrimidinyl-piperazine). Herein, we examined mechanisms underlying the influence of buspirone alone, and in association with the serotonin reuptake inhibitor, fluoxetine, upon extracellular levels of serotonin, dopamine and noradrenaline simultaneously quantified in the frontal cortex of freely moving rats. Buspirone (0.01-2.5 mg/kg, s.c.) dose-dependently decreased dialysate levels of serotonin (-50%), and increased those of dopamine (+100%) and noradrenaline (+140%). The reduction by buspirone of serotonin levels was abolished by the serotonin1A receptor antagonist, WAY 100,635 (0.16), which did not, however, modify its influence upon dopamine and noradrenaline. In contrast to buspirone, the serotonin reuptake inhibitor, fluoxetine (10.0), increased frontocortical levels of serotonin (+ 120%), dopamine (+55%) and noradrenaline (+90%). Buspirone dose-dependently (0.01-2.5) decreased the induction by fluoxetine of serotonin levels yet potentiated (three-fold) its elevation of dopamine and noradrenaline levels. The serotonin1A agonist, 8-hydroxy-2-(di-n-propyl-amino)-tetralin (0.16), mimicked the action of buspirone in reducing resting levels of serotonin (-60%) and in enhancing those of dopamine (+135%) and noradrenaline (+165%). Like buspirone, it attenuated the influence of fluoxetine upon serotonin levels, yet facilitated its influence upon dopamine and noradrenaline levels. In contrast, WAY 100,635 selectively potentiated the increase in levels of serotonin (two-fold) versus dopamine and noradrenaline elicited by fluoxetine. Further, WAY 100,635 abolished the inhibitory influence of buspirone upon fluoxetine-induced serotonin release, but only partly interfered with its potentiation of fluoxetine-induced increases in dopamine and noradrenaline levels. The D2/D3 receptor antagonist, raclopride (0.16), increased basal dopamine (+60%) levels but little influenced those of serotonin and noradrenaline, and failed to modify the action of fluoxetine. The alpha2-adrenergic receptor antagonist, 1-(2-pyrimidinyl-piperazine) (2.5), which did not modify resting levels of serotonin, markedly increased those of dopamine (+90%) and noradrenaline (+190%) and potentiated (two-fold) the increases in dialysate levels of dopamine, noradrenaline and serotonin provoked by fluoxetine. Further, the alpha2-adrenergic receptor agonist, S18616, attenuated the enhancement by buspirone of the fluoxetine-induced increase in levels of dopamine and noradrenaline. In conclusion, the inhibitory influence of buspirone upon resting and fluoxetine-stimulated serotonin levels reflects its agonist properties at serotonin1A autoreceptors. The facilitatory influence of buspirone upon resting and fluoxetine-stimulated dopamine and noradrenaline levels may also involve its serotonin1A properties. However, its principal mechanism of action in this respect is probably the alpha2-adrenergic antagonist properties of its metabolite, 1-(2-pyrimidinyl-piperazine). The present observations are of significance to experimental and clinical studies of the influence of buspirone upon depressive states, alone and in association with antidepressant agents.
PMID: 10501449 [PubMed - indexed for MEDLINE]
> If it was making your temper or mood worse to a point where you couldn't function, then it probably was best to go off it (without any need to speculate about the mechanism whereby it did this). What dose were you taking, and for how long?
>
> -elizabeth
Posted by AMenz on July 9, 2001, at 10:52:07
In reply to Re: Going Crazy: Could it be Buspar????? » Elizabeth, posted by Mitch on July 8, 2001, at 16:45:45
Let's take this a step at a time. Please help me here.
"Buspirone (0.01-2.5 mg/kg, s.c.) dose-dependently decreased dialysate levels of serotonin (-50%), and increased those of dopamine (+100%) and noradrenaline (+140%)."Also what is WAY 100,635 and why are they mentioning it here if they are doing a comparison of fluoxetine and buspirone alone and in combination?
"The reduction by buspirone of serotonin levels was abolished by the serotonin1A receptor antagonist, WAY 100,635 (0.16), which did not, however, modify its influence upon dopamine and noradrenaline."
Next fluoxetine increases extracellelar levels of serotonin:
"In contrast to buspirone, the serotonin reuptake inhibitor, fluoxetine (10.0), increased frontocortical levels of serotonin (+ 120%), dopamine (+55%) and noradrenaline (+90%)."
Together Buspirone reduces the serotonin levels as enhanced alone by fluoxetine:
"Buspirone dose-dependently (0.01-2.5) decreased the induction by fluoxetine of serotonin levels yet potentiated (three-fold) its elevation of dopamine and noradrenaline levels."
But then you come to the agonist properties of buspirone at the serotonin1A receptor. What does this entail? Does it increase certain intracellular activity because it mimics seratonin so that the cell acts as if seratonin were enhanced instead of diminished?
"In conclusion, the inhibitory influence of buspirone upon resting and fluoxetine-stimulated serotonin levels reflects its agonist properties at serotonin1A autoreceptors. The facilitatory influence of buspirone upon resting and fluoxetine-stimulated dopamine and noradrenaline levels may also involve its serotonin1A properties."
OK so my questions in closing are:1)what is the consequence of this mimicking effect.
2) more seratonin equals more mania and less seratonin depression
3) do they have any idea as to effect of dopamine and noradrenaline on mood?
Thanks for any help with these questions. ARe doctors reluctant to discuss these issues because they think their patients are too stupid or because they themselves don't read?
Posted by Mitch on July 9, 2001, at 13:30:49
In reply to Re: Going Crazy: Could it be Buspar????? Mitch, posted by AMenz on July 9, 2001, at 10:52:07
> Let's take this a step at a time. Please help me here.
> "Buspirone (0.01-2.5 mg/kg, s.c.) dose-dependently decreased dialysate levels of serotonin (-50%), and increased those of dopamine (+100%) and noradrenaline (+140%)."Well, for starters I didn't write the thing! It appears they are administering buspirone to mice/rats and then seeing what happens to the extracellular neurotransmitters in their brains in response to the administration.
>
> Also what is WAY 100,635 and why are they mentioning it here if they are doing a comparison of fluoxetine and buspirone alone and in combination?It is an investigational drug that has very specific actions that they can use as a comparison/control. I think most meds have their beginning named like that until they are further developed. When this article was written there was a lot of success stories about augmenting SSRI antidepressants with buspirone and I think their findings here (and other people's anecdotal findings with humans)is the reason for the comparison of buspirone alone and with fluoxetine. I am sensitive to AD's and I was taking an SSRI at the time (Celexa), and it sure boosted it alright!
>
> "The reduction by buspirone of serotonin levels was abolished by the serotonin1A receptor antagonist, WAY 100,635 (0.16), which did not, however, modify its influence upon dopamine and noradrenaline."The investigational drug WAY... when given along with buspirone kept buspirone from reducing serotonin levels (blocked Buspar's anti-serotonin activity). But buspirone still boosted dopamine and norepinephrine levels despite that.
>
> Next fluoxetine increases extracellelar levels of serotonin:Prozac is an SSRI drug that blocks the "pumps" that take extra serotonin in the synapses and removes it. If you block the pump that removes the serotonin from the synapse then it accumulates to a higher level-that is basically how SSRi's are supposed to work (from what I understand).
>
> "In contrast to buspirone, the serotonin reuptake inhibitor, fluoxetine (10.0), increased frontocortical levels of serotonin (+ 120%), dopamine (+55%) and noradrenaline (+90%)."That is just the result of Prozac being admininstered alone (the extra-cellular concentrations of the three neurotransmitters mentioned). Obviously there are boosts in other transmitters besides serotonin due to fluoxetine.
>
> Together Buspirone reduces the serotonin levels as enhanced alone by fluoxetine:Buspirone simply thwarts or reverses the serotonin increase that fluoxetine causes.
>
> "Buspirone dose-dependently (0.01-2.5) decreased the induction by fluoxetine of serotonin levels yet potentiated (three-fold) its elevation of dopamine and noradrenaline levels."The trick here is that when buspirone was coadministered with Prozac you get a *potentiation* of dopamine and norepinephrine. That wouldn't have happened if you just administered Prozac.
>
> But then you come to the agonist properties of buspirone at the serotonin1A receptor. What does this entail? Does it increase certain intracellular activity because it mimics seratonin so that the cell acts as if seratonin were enhanced instead of diminished?That sounds like a plausible explanation-better than what I could have conjectured. Perhaps *synthesis* of serotonin is also decreased as a result. Possible analogy?? (it seems like we got plenty why make more??)
>
> "In conclusion, the inhibitory influence of buspirone upon resting and fluoxetine-stimulated serotonin levels reflects its agonist properties at serotonin1A autoreceptors. The facilitatory influence of buspirone upon resting and fluoxetine-stimulated dopamine and noradrenaline levels may also involve its serotonin1A properties."Good question. I can see I think how it can reduce serotonin-but there is some extra hidden complexity (of course) that explains the NE and DA boost.
> OK so my questions in closing are:
>
> 1)what is the consequence of this mimicking effect.It reduces jitteriness (less serotonin)-which is what happens during startup of taking SSRi's-you get all restless and jittery (lots of extra serotonin until your receptor density changes -from what I have read here anyway).
>
> 2) more seratonin equals more mania and less seratonin depressionQuite possibly.
Personally, I think it has more to do with the relative balance between the neurotransmitters. Some people respond better to certain AD's better than others. Basically, I think that pitching in Buspirone with an SSRi-turns the combination into more of an Effexor-like response. I have become hypomanic on very selective SSRi's (at higher doses), while a tiny dose of Effexor can make me very hypomanic.
>
> 3) do they have any idea as to effect of dopamine and noradrenaline on mood?Well, from what my pdoc has mentioned (very generally), dopamine is involved with interest and Norepi with drive and energy. Serotonin has the most to do with "mood".
>
> Thanks for any help with these questions. ARe doctors reluctant to discuss these issues because they think their patients are too stupid or because they themselves don't read?I think it is a two-fold problem. A lot of doctors don't keep up with literature-especially nowadays with the acceleration in the amount of knowledge with respect to psychopharmacology. And newer drugs coming out every month doesn't help paradoxically-it increases the number of choices complicating treatment (for a doc that is not staying on top of it).
I don't think that doctors think all their patients are too stupid. Several docs have told me they don't have the time to waste to explain how the drug is supposed to work-and if they get too involved explaining then patients may get too focused on side effects rather than their improvement as a result of the med.
Posted by AMenz on July 12, 2001, at 13:19:00
In reply to Re: Going Crazy: Could it be Buspar????? Mitch » AMenz, posted by Mitch on July 9, 2001, at 13:30:49
Thank you for your response. I must say that the study left me perplexed as to how Buspar and SSRI's in combination could cause hypomania. I take it that there is no real understanding of what the mimicking effect is. I thought the mimicking effect would be the answer to the conondrum since it might explain hypomania when serotonin levels were actually lowered.
If when Buspar and SSRI's are administered conjointly the end result is that there is less serotonin potentiation (is this the right word?) than when SSRI is administered alone, I see no explanation for the concomitant hypomania, unless at least one of the following is true:(a) an increase in serotonin levels alone is not the cause of hypomania, {here serotonin was decreased but hypomania ensued].
(b) the mimicking action creates an "as if" condition, so that the brain responds as if serotonin had increased, rather than decreased as is the case.
c) Hypomania as you say is caused by the relative levels of the neurotransmitters as opposed to the absolute level to seratonin. One would then have to conclude that higher levels of NE and/or Dopamine relative to serotonin causes hypomania.
Well, I guess my frustration is that I simply do not see that my several practitioners understand any of these interactions any better than I do. At this point I don't think I am willing to try any further combinations of anything.
I agree with you that the plethora of medication make it mathematically less probable that a particular combination that is favorable will be found. I've been thinking about this for quite a while.
I also think that the continuous switching of medications and adjusting dosages willy nilly accounts for the worsening of symptoms with some patients (moi for instance) insofar as stasis is whats lacking in the brain of the bipolar. I cannot think of anything more destabilizing than ripping of Lithium, then conducting trials with Lamictal, Neurontin, Topomax in the space of less than six months.
These people have done me a great disservice and they are not liable for malpractice in my state unless the damage they cause is permanent.
I am really angry.
Thanks for your very careful response. It was very helpful.
> > Let's take this a step at a time. Please help me here.
> > "Buspirone (0.01-2.5 mg/kg, s.c.) dose-dependently decreased dialysate levels of serotonin (-50%), and increased those of dopamine (+100%) and noradrenaline (+140%)."
>
> Well, for starters I didn't write the thing! It appears they are administering buspirone to mice/rats and then seeing what happens to the extracellular neurotransmitters in their brains in response to the administration.
> >
> > Also what is WAY 100,635 and why are they mentioning it here if they are doing a comparison of fluoxetine and buspirone alone and in combination?
>
> It is an investigational drug that has very specific actions that they can use as a comparison/control. I think most meds have their beginning named like that until they are further developed. When this article was written there was a lot of success stories about augmenting SSRI antidepressants with buspirone and I think their findings here (and other people's anecdotal findings with humans)is the reason for the comparison of buspirone alone and with fluoxetine. I am sensitive to AD's and I was taking an SSRI at the time (Celexa), and it sure boosted it alright!
> >
> > "The reduction by buspirone of serotonin levels was abolished by the serotonin1A receptor antagonist, WAY 100,635 (0.16), which did not, however, modify its influence upon dopamine and noradrenaline."
>
> The investigational drug WAY... when given along with buspirone kept buspirone from reducing serotonin levels (blocked Buspar's anti-serotonin activity). But buspirone still boosted dopamine and norepinephrine levels despite that.
> >
> > Next fluoxetine increases extracellelar levels of serotonin:
>
> Prozac is an SSRI drug that blocks the "pumps" that take extra serotonin in the synapses and removes it. If you block the pump that removes the serotonin from the synapse then it accumulates to a higher level-that is basically how SSRi's are supposed to work (from what I understand).
> >
> > "In contrast to buspirone, the serotonin reuptake inhibitor, fluoxetine (10.0), increased frontocortical levels of serotonin (+ 120%), dopamine (+55%) and noradrenaline (+90%)."
>
> That is just the result of Prozac being admininstered alone (the extra-cellular concentrations of the three neurotransmitters mentioned). Obviously there are boosts in other transmitters besides serotonin due to fluoxetine.
> >
> > Together Buspirone reduces the serotonin levels as enhanced alone by fluoxetine:
>
> Buspirone simply thwarts or reverses the serotonin increase that fluoxetine causes.
> >
> > "Buspirone dose-dependently (0.01-2.5) decreased the induction by fluoxetine of serotonin levels yet potentiated (three-fold) its elevation of dopamine and noradrenaline levels."
>
> The trick here is that when buspirone was coadministered with Prozac you get a *potentiation* of dopamine and norepinephrine. That wouldn't have happened if you just administered Prozac.
> >
> > But then you come to the agonist properties of buspirone at the serotonin1A receptor. What does this entail? Does it increase certain intracellular activity because it mimics seratonin so that the cell acts as if seratonin were enhanced instead of diminished?
>
> That sounds like a plausible explanation-better than what I could have conjectured. Perhaps *synthesis* of serotonin is also decreased as a result. Possible analogy?? (it seems like we got plenty why make more??)
> >
> > "In conclusion, the inhibitory influence of buspirone upon resting and fluoxetine-stimulated serotonin levels reflects its agonist properties at serotonin1A autoreceptors. The facilitatory influence of buspirone upon resting and fluoxetine-stimulated dopamine and noradrenaline levels may also involve its serotonin1A properties."
>
> Good question. I can see I think how it can reduce serotonin-but there is some extra hidden complexity (of course) that explains the NE and DA boost.
>
> > OK so my questions in closing are:
> >
> > 1)what is the consequence of this mimicking effect.
>
> It reduces jitteriness (less serotonin)-which is what happens during startup of taking SSRi's-you get all restless and jittery (lots of extra serotonin until your receptor density changes -from what I have read here anyway).
> >
> > 2) more seratonin equals more mania and less seratonin depression
>
> Quite possibly.
>
> Personally, I think it has more to do with the relative balance between the neurotransmitters. Some people respond better to certain AD's better than others. Basically, I think that pitching in Buspirone with an SSRi-turns the combination into more of an Effexor-like response. I have become hypomanic on very selective SSRi's (at higher doses), while a tiny dose of Effexor can make me very hypomanic.
> >
> > 3) do they have any idea as to effect of dopamine and noradrenaline on mood?
>
> Well, from what my pdoc has mentioned (very generally), dopamine is involved with interest and Norepi with drive and energy. Serotonin has the most to do with "mood".
> >
> > Thanks for any help with these questions. ARe doctors reluctant to discuss these issues because they think their patients are too stupid or because they themselves don't read?
>
> I think it is a two-fold problem. A lot of doctors don't keep up with literature-especially nowadays with the acceleration in the amount of knowledge with respect to psychopharmacology. And newer drugs coming out every month doesn't help paradoxically-it increases the number of choices complicating treatment (for a doc that is not staying on top of it).
>
> I don't think that doctors think all their patients are too stupid. Several docs have told me they don't have the time to waste to explain how the drug is supposed to work-and if they get too involved explaining then patients may get too focused on side effects rather than their improvement as a result of the med.
Posted by Mitch on July 12, 2001, at 23:58:55
In reply to Re: Going Crazy: Could it be Buspar????? Mitch, posted by AMenz on July 12, 2001, at 13:19:00
AMenz,
> I must say that the study left me perplexed as to how Buspar and SSRI's in combination could cause hypomania.
I don't think that Buspar per se is a *culprit* necessarily. I just think that the combo of Buspar+SSRI is a STRATEGY to treat people who are not showing a response to SSRi alone for UNIPOLAR depression. I just think the study shows that Buspar has a way of boosting other neurotransmitters that can help someone who is treatment-resistant for severe depression. SOMEONE WHO IS BIPOLAR SHOULD ALWAYS BE CAREFUL about what AD's they take and what agents are used to augment them. In my case I was just taking some Buspar to help reduce *anxiety* NOT to boost antidepressant response of the SSRi I was also taking.
>
> If when Buspar and SSRI's are administered conjointly the end result is that there is less serotonin potentiation (is this the right word?) than when SSRI is administered alone, I see no explanation for the concomitant hypomania, unless at least one of the following is true:
>
> (a) an increase in serotonin levels alone is not the cause of hypomania, {here serotonin was decreased but hypomania ensued].
>
> (b) the mimicking action creates an "as if" condition, so that the brain responds as if serotonin had increased, rather than decreased as is the case.
>
> c) Hypomania as you say is caused by the relative levels of the neurotransmitters as opposed to the absolute level to seratonin. One would then have to conclude that higher levels of NE and/or Dopamine relative to serotonin causes hypomania.This is a complex interaction between the SSRI and buspirone. It depends on the RELATIVE dose of EACH med and the person. Basically, I think it is the big boost in NE and DA that caused the irritability with me. You see I was taking a TINY dose of SSRi and added a NOT AS TINY dose of buspirone-so given my combination-I probably ended up with a NET decrease of serotonin (making me grouchy) and a BIG boost in NE and DA which made me all wired up. Which could be a magical response to someone resistant to treatment for pure depression.
>
> Well, I guess my frustration is that I simply do not see that my several practitioners understand any of these interactions any better than I do. At this point I don't think I am willing to try any further combinations of anything.I think you may be too pessimistic-although I understand your frustration!! This was just a *remarkable* combination in a bipolar person who is sensitive to AD's. There is an element of experimentation that has to take place to *find out* what is going to work for you and unfortunately at times what ISN"T going to work.
>
> I agree with you that the plethora of medication make it mathematically less probable that a particular combination that is favorable will be found. I've been thinking about this for quite a while.This possibly (hopefully!) could be a relatively short-term phenomenon until more selectively designed meds can come into the market (with the help of genomics).
>
> I also think that the continuous switching of medications and adjusting dosages willy nilly accounts for the worsening of symptoms with some patients (moi for instance) insofar as stasis is whats lacking in the brain of the bipolar. I cannot think of anything more destabilizing than ripping of Lithium, then conducting trials with Lamictal, Neurontin, Topomax in the space of less than six months.Some doctors want to get away from older more dangerous or toxic drugs such as Lithium, tricyclics, MAOI's for example. They might work for you, but what shape will your liver, kidneys, pancreas, etc. be in another 10 years?? Also, if you got very suicidal during a depressive episode (which say only lasted a few weeks) and chucked a bottle of Lithium or tricyclics and croaked-you wouldn't be around for a better future treatment would you??
>
> These people have done me a great disservice and they are not liable for malpractice in my state unless the damage they cause is permanent.
>
> I am really angry.This is a transitional period where doctors/patients/pharmaceutical co's are needing increased education and access to information to improve treatment. You have to remember that some of the meds that are just coming out have been under investigation for many years. I may sound a little apologetic for bad docs or greedy drug companies, but I am optimistic about the future of treatment. It is just a real thicket right now-and you are more likely to get bad medcombos for the time being until the pdocs catch up with and stay with all the new stuff.
Mitch
This is the end of the thread.
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