![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 20 of 20. This is the beginning of the thread.
Posted by JohnX on October 13, 2001, at 17:19:01
Is zyprexa primarily a presynaptic
dopamine antagonist at low doses?At what doses is it effective for
anxiety/depression, and at what dosing
point do we get into anti-psychotic land?Thanks for any info,
John
Posted by Collete on October 14, 2001, at 0:37:46
In reply to zyprexa dose, posted by JohnX on October 13, 2001, at 17:19:01
>
> Is zyprexa primarily a presynaptic
> dopamine antagonist at low doses?
>
> At what doses is it effective for
> anxiety/depression, and at what dosing
> point do we get into anti-psychotic land?
>
> Thanks for any info,
> John
I don't know about the AP dose, but my pdoc started me on just 2.5mg for depression ( along with continuing my 20 mg of Prozac) and it worked immediately. John L said that one usually knows within a week if it is going to help them.
HTH, Collette
Posted by Cam W. on October 14, 2001, at 2:18:55
In reply to zyprexa dose, posted by JohnX on October 13, 2001, at 17:19:01
John - Zyprexa™ (olanzapine) is mainly a postsynaptic dopamine-D2 (D2) receptor blocker (as well as blocking other postsynaptic dopamine, serotonin, and muscarinic receptors). An interesting theory was put forth by Dr. Phil Seeman (the guy who invented the receptor site theory) at an "Update on the Management of Psychosis" conference that I attended a couple of years ago. He claimed that the reason that it "appears" that the atypical antipsychotics have low binding constant is because they don't irreversibly bind to the postsynaptic D2 receptor, but rather they "tweak" this receptor. This allows for multiple tweakings of the receptor, leading to better modulation of dopamine neurotransmission, permitting an antipsychotic effect without motor side effects (EPS and TD), prolactin elevation, or secondary negative symptoms. He also said that this tweaking, in itself, is sufficient for the antipsychotic effect of the atypicals. He subsequently went on the publish this theory in two extrordinary articles:
1) Seeman, P. "Antipsychotic Drugs, Dopamine Receptors, and Schizophrenia", Clinical Neuroscience Research, 2001, 1: 53-60.
2) Kapur, S., Seeman, P. "Does Fast Dissociation From the Dopamine D2 Receptor Explain the Action of Atypical Antipsychotics?: A New Hypothesis", American Jounral of Psychiatry, 2001, 158: 360-369.
In the second article, Kapur (a brilliant man - and speaker) and Seeman conclude that the blocade of the serotonin-2A (5-HT2A) and the dopamine-D4 (D4) receptor do not contribute to antipsychotic activity.
But, at the Edmonton Schizophrenia 2001 Conference on Friday, Dr. Susan McGurk stated that the the dopamine-D1 receptor blockade by atypical antipsychotics may conceivably increase dopamine turnover in the prefrontal cortex, thus contributing to the increase in cognition see with these agents. She stated that the increase in dopamine in the prefrontal cortex offsets the decrease in cognition caused by the muscarinic-M1 (M1) receptor blocking action of Zyprexa. She also said that another explanation of a lack of cognitive dulling by Zyprexa could be due to the blocking of only select subtypes of the M1 receptor. Dr. McGurk also stated that the reason that Risperdal™ (risperidone) improves many areas of cognition better tha Zyprexa, is because Risperdal is devoid of M1 receptor blockade. Only Clozaril™ (clozapine) has shown to cause cognitive blunting due to it's built-in antimuscarinic action, due to it's blocking of acetylcholine receptors in frontal brain areas, which does not offset the Clozaril-induced increase in dopamine in this location.
Another interesting bit of information that she shared (and that I wasn't aware of) was that the older typical antipsychotics have very little direct effect on cognition. I had always assumed that they did cause cognitive blunting. Dr. McGurk said that because typical antipsychotics cause EPS, people taking them usually need to take a muscarinic blocker like Cogentin™ (benztropine) or Artane™ (trihexyphenidyl), and it is these that cause the cognitive problems.
As to Zyprexa dosing, Friday, Dr. Bill Honer, his plenary talk that I attended, commented on an article published last year in the European Journal of Pharmacology (? - I think - I haven't looked for it yet, and, of course, I missed writing down the author's and the journal names) which stated that maximal effective dosages of Zyprexa in psychosis were less in women (approx 13mg) than in men (approx. 17mg), above which, in most people, there will not be an increase in efficacy. Dr. Honer also stated that Zyprexa for augmentaion of unipolar depression or bipolar disorder, but not psychotic depression, usually required lower doses, but since it is difficult to predict how much less of a dose one would use in these two disorders because dosing with Zyprexa is very individualized. The way he approaches it is to start with 2.5mg or 5 mg of Zyprexa or 0.5 to 2mg of Risperdal (depending on the extent of response of the primary agent being used) and to increase slowly, as necessary.
I hope that this rambling (and unabashed name-dropping) is of some help. - Cam
Posted by ChrisK on October 14, 2001, at 5:16:27
In reply to zyprexa dose, posted by JohnX on October 13, 2001, at 17:19:01
My pdoc trusts me with meds so he started me out with a suply of 2.5 mg Zyprexa and told me to experiment with dosage until I found one that suited me. After about a month or two of trials I landed on 7.5 mg taken at night. I probably could go back to 5 mg without a noticable difference in my treatment but I've been on the 7.5 so long we are just leaving it there.
I'm pretty sure that I've read here and elsewhere that the anti-psychotic doses start above 10 mg. I know one of the clients where I work who is autistic with psychosis takes 15 mg of Zyprexa once per day.
Posted by NikkiT2 on October 14, 2001, at 7:24:30
In reply to Re: zyprexa dose » JohnX, posted by Cam W. on October 14, 2001, at 2:18:55
Fab post Cam!!! I even understood most of it!!
Thanks for that info... You're a top geezer!! :o)
Nikki xx
Posted by Collete on October 14, 2001, at 10:02:17
In reply to Re: zyprexa dose » Cam W., posted by NikkiT2 on October 14, 2001, at 7:24:30
> Fab post Cam!!! I even understood most of it!!
>
> Thanks for that info... You're a top geezer!! :o)
>
> Nikki xxZyprexa was amazing for me at 2.5 but the overeating was a big problem. Geodon is out because it costs a fortune and I can't get it any cheaper through Canadadrugs.com. Based on that, is there any reason for me to try Lamictal instead of trying Zyprexa again with yet another med(Topamax) to control appetite? I guess I am wondering if you can explain in layman's terms how Lamictal works. THANKS! Collette
Posted by Cam W. on October 14, 2001, at 23:28:38
In reply to Cam, me too ,,,what Nikki said! lol, posted by Collete on October 14, 2001, at 10:02:17
> I guess I am wondering if you can explain in layman's terms how Lamictal works. THANKS! Collette
Collete - For what diagnosis are you potentially taking these medications? It can help to tailor my answer. BTW - Give me a few days to formulate an answer; I am working a 5 days/55 hour stretch, and am really too tired to put the proper effort into formulating an proper answer. - Cam
Posted by JohnX on October 15, 2001, at 23:53:02
In reply to Re: zyprexa dose » JohnX, posted by Cam W. on October 14, 2001, at 2:18:55
> John - Zyprexa™ (olanzapine) is mainly a postsynaptic dopamine-D2 (D2) receptor blocker (as well as blocking other postsynaptic dopamine, serotonin, and muscarinic receptors). An interesting theory was put forth by Dr. Phil Seeman (the guy who invented the receptor site theory) at an "Update on the Management of Psychosis" conference that I attended a couple of years ago. He claimed that the reason that it "appears" that the atypical antipsychotics have low binding constant is because they don't irreversibly bind to the postsynaptic D2 receptor, but rather they "tweak" this receptor. This allows for multiple tweakings of the receptor, leading to better modulation of dopamine neurotransmission, permitting an antipsychotic effect without motor side effects (EPS and TD), prolactin elevation, or secondary negative symptoms. He also said that this tweaking, in itself, is sufficient for the antipsychotic effect of the atypicals. He subsequently went on the publish this theory in two extrordinary articles:
>
> 1) Seeman, P. "Antipsychotic Drugs, Dopamine Receptors, and Schizophrenia", Clinical Neuroscience Research, 2001, 1: 53-60.
>
> 2) Kapur, S., Seeman, P. "Does Fast Dissociation From the Dopamine D2 Receptor Explain the Action of Atypical Antipsychotics?: A New Hypothesis", American Jounral of Psychiatry, 2001, 158: 360-369.
>
> In the second article, Kapur (a brilliant man - and speaker) and Seeman conclude that the blocade of the serotonin-2A (5-HT2A) and the dopamine-D4 (D4) receptor do not contribute to antipsychotic activity.
>
> But, at the Edmonton Schizophrenia 2001 Conference on Friday, Dr. Susan McGurk stated that the the dopamine-D1 receptor blockade by atypical antipsychotics may conceivably increase dopamine turnover in the prefrontal cortex, thus contributing to the increase in cognition see with these agents. She stated that the increase in dopamine in the prefrontal cortex offsets the decrease in cognition caused by the muscarinic-M1 (M1) receptor blocking action of Zyprexa. She also said that another explanation of a lack of cognitive dulling by Zyprexa could be due to the blocking of only select subtypes of the M1 receptor. Dr. McGurk also stated that the reason that Risperdal™ (risperidone) improves many areas of cognition better tha Zyprexa, is because Risperdal is devoid of M1 receptor blockade. Only Clozaril™ (clozapine) has shown to cause cognitive blunting due to it's built-in antimuscarinic action, due to it's blocking of acetylcholine receptors in frontal brain areas, which does not offset the Clozaril-induced increase in dopamine in this location.
>
> Another interesting bit of information that she shared (and that I wasn't aware of) was that the older typical antipsychotics have very little direct effect on cognition. I had always assumed that they did cause cognitive blunting. Dr. McGurk said that because typical antipsychotics cause EPS, people taking them usually need to take a muscarinic blocker like Cogentin™ (benztropine) or Artane™ (trihexyphenidyl), and it is these that cause the cognitive problems.
>
> As to Zyprexa dosing, Friday, Dr. Bill Honer, his plenary talk that I attended, commented on an article published last year in the European Journal of Pharmacology (? - I think - I haven't looked for it yet, and, of course, I missed writing down the author's and the journal names) which stated that maximal effective dosages of Zyprexa in psychosis were less in women (approx 13mg) than in men (approx. 17mg), above which, in most people, there will not be an increase in efficacy. Dr. Honer also stated that Zyprexa for augmentaion of unipolar depression or bipolar disorder, but not psychotic depression, usually required lower doses, but since it is difficult to predict how much less of a dose one would use in these two disorders because dosing with Zyprexa is very individualized. The way he approaches it is to start with 2.5mg or 5 mg of Zyprexa or 0.5 to 2mg of Risperdal (depending on the extent of response of the primary agent being used) and to increase slowly, as necessary.
>
> I hope that this rambling (and unabashed name-dropping) is of some help. - CamCam,
This is really good. Thanks for your time and
effort to piece this together.I ramble at least as well as you; no biggie.
More info the better!Regards,
john
Posted by JohnX on October 16, 2001, at 1:48:06
In reply to Re: zyprexa dose » JohnX, posted by Cam W. on October 14, 2001, at 2:18:55
> John - Zyprexa™ (olanzapine) is mainly a postsynaptic dopamine-D2 (D2) receptor blocker (as well as blocking other postsynaptic dopamine, serotonin, and muscarinic receptors). An interesting theory was put forth by Dr. Phil Seeman (the guy who invented the receptor site theory) at an "Update on the Management of Psychosis" conference that I attended a couple of years ago. He claimed that the reason that it "appears" that the atypical antipsychotics have low binding constant is because they don't irreversibly bind to the postsynaptic D2 receptor, but rather they "tweak" this receptor. This allows for multiple tweakings of the receptor, leading to better modulation of dopamine neurotransmission, permitting an antipsychotic effect without motor side effects (EPS and TD), prolactin elevation, or secondary negative symptoms. He also said that this tweaking, in itself, is sufficient for the antipsychotic effect of the atypicals. He subsequently went on the publish this theory in two extrordinary articles:
>
> 1) Seeman, P. "Antipsychotic Drugs, Dopamine Receptors, and Schizophrenia", Clinical Neuroscience Research, 2001, 1: 53-60.
>
> 2) Kapur, S., Seeman, P. "Does Fast Dissociation From the Dopamine D2 Receptor Explain the Action of Atypical Antipsychotics?: A New Hypothesis", American Jounral of Psychiatry, 2001, 158: 360-369.
>
> In the second article, Kapur (a brilliant man - and speaker) and Seeman conclude that the blocade of the serotonin-2A (5-HT2A) and the dopamine-D4 (D4) receptor do not contribute to antipsychotic activity.
>
> But, at the Edmonton Schizophrenia 2001 Conference on Friday, Dr. Susan McGurk stated that the the dopamine-D1 receptor blockade by atypical antipsychotics may conceivably increase dopamine turnover in the prefrontal cortex, thus contributing to the increase in cognition see with these agents. She stated that the increase in dopamine in the prefrontal cortex offsets the decrease in cognition caused by the muscarinic-M1 (M1) receptor blocking action of Zyprexa. She also said that another explanation of a lack of cognitive dulling by Zyprexa could be due to the blocking of only select subtypes of the M1 receptor. Dr. McGurk also stated that the reason that Risperdal™ (risperidone) improves many areas of cognition better tha Zyprexa, is because Risperdal is devoid of M1 receptor blockade. Only Clozaril™ (clozapine) has shown to cause cognitive blunting due to it's built-in antimuscarinic action, due to it's blocking of acetylcholine receptors in frontal brain areas, which does not offset the Clozaril-induced increase in dopamine in this location.
>
> Another interesting bit of information that she shared (and that I wasn't aware of) was that the older typical antipsychotics have very little direct effect on cognition. I had always assumed that they did cause cognitive blunting. Dr. McGurk said that because typical antipsychotics cause EPS, people taking them usually need to take a muscarinic blocker like Cogentin™ (benztropine) or Artane™ (trihexyphenidyl), and it is these that cause the cognitive problems.
>
> As to Zyprexa dosing, Friday, Dr. Bill Honer, his plenary talk that I attended, commented on an article published last year in the European Journal of Pharmacology (? - I think - I haven't looked for it yet, and, of course, I missed writing down the author's and the journal names) which stated that maximal effective dosages of Zyprexa in psychosis were less in women (approx 13mg) than in men (approx. 17mg), above which, in most people, there will not be an increase in efficacy. Dr. Honer also stated that Zyprexa for augmentaion of unipolar depression or bipolar disorder, but not psychotic depression, usually required lower doses, but since it is difficult to predict how much less of a dose one would use in these two disorders because dosing with Zyprexa is very individualized. The way he approaches it is to start with 2.5mg or 5 mg of Zyprexa or 0.5 to 2mg of Risperdal (depending on the extent of response of the primary agent being used) and to increase slowly, as necessary.
>
> I hope that this rambling (and unabashed name-dropping) is of some help. - CamCam,
Would you have an idea as to why I felt so
drugged out on Serzone and not nearly as bad
on Zyprexa (if at all noticeable). I wasn't taking
Lamictal when I took Serzone. Now I am taking
Lamictal (150mg) with Zyprexa (5mg).When I took Serzone, my life was a blurr. I felt
like I was always drunk, and I rear-ended someone,
which stopped me from taking the med. It did have
an awesome improvement in my sleep and releived
anhedonia (although I was to tired to have fun).
I told myself I would never take Serzone again,
but I don't even remember why that's how foggy
my brain was. I was worried Zyprexa would do the
same, but it hasn't.Also, any ballpark estimate for TD possiblity
on Zyprexa? I take some anti-oxidants, but I
don't know if they help (like Vitamin E). I understand
there could be interactions with anything that
inhibits a particular enzyme cyp 450-1a2? (the caffeine one,
my brain fog elludes me), so I shouldn't take
some herbs like Valerian which I occasionally take
for sleep.Thanks for your great help.
-John
Posted by Cam W. on October 17, 2001, at 2:33:22
In reply to Re: zyprexa dose » Cam W., posted by JohnX on October 16, 2001, at 1:48:06
John - I have always found Serzone™ (nefazodone) to be a weird drug. It seems either really work well as an antidepressant, or not at all. I think that the serotonin-2 (5-HT2) blocking ability of the drug has a lot to do with it's ability to really screw-up some people. It's adverse actions in some people may have to do with the relative concentrations and locations of 5-HT2 receptors in these people.
Perhaps the "fogginess" that you experienced had something to do with Serzone's action in the reticular activating system (RAS); the part of the brain responsible for the sleep/wake mechanisms of the body. The RAS contains the raphe nuclei, which is the part of the brain with the densest concentration of serotonin receptors, so this might be the reason why Serzone works so well in improving "sleep architecture" (ie. Serzone supposedly "normalizes" the different stages of sleep). Perhaps the blocking of certain serotonin receptor subtypes in this area buggering up your sleep/wake cycle and the fogginess might be due to your brain being stuck in one of the stages of sleep, while you are awake (caveat - this is just me thinking out loud, and is a total guess on my part).
Serzone is a very potent inhibitor of CYP-3A3 and CYP-3A4 (which are closely linked), but it also inhibits, to a lesser extent, CYP-2D6 and CYP-1A2. Therefore it has the potential to increase plasma concentration of an incredibly wide range of medications, including caffeine. As for affecting herbs, the only one that I can think of affecting, off of the top of my head, is St.John's Wort.
The incidence of contracting tardive dyskinesia (TD) from Zyprexa™ (olanzapine) is very low, probably due to it's "tweaking" of the dopamine-2 (D2) receptor (rather than binding irreversibly to it, like the traditional antipsychotics do). Risperdal™ (risperidone), at higher doses ( >6mg/day) causes EPS, because it seems to bind tighter (although still less than most traditonals) to D2 receptors, and doses over 6mg/day seems to saturate D2 receptors in the basal ganglia more so than other atypicals
Also, I think that quite a few of the cases of TD reported to be caused by Zyprexa were, in actuality, the "unmasking" of TD caused by past traditional antipsychotic use. In some cases, traditional antipsychotics and anticholinergics (like Cogentin™ - benztropine) seem to hide the TD. Once these suseptible people switch to Zyprexa, the TD emerges. Again, I have no proof of this, other than what I have seen clinically. I was looking after one gentleman who had some mild signs of TD while taking Orap™ (pimozide) and Artane™ (trihexyphendyl). and when he was switched to Zyprexa, the TD came out with a vengence (ie. his tongue started flicking in and out of his mouth rapidly, all day, every day, while awake. In itself, Zyprexa seems not to cause TD very often at all.
Again, this post is full of guesses and musings, but no real, proven hard facts. - Cam
Posted by JohnX on October 17, 2001, at 10:23:13
In reply to Re: zyprexa dose, posted by Cam W. on October 17, 2001, at 2:33:22
> John - I have always found Serzone™ (nefazodone) to be a weird drug. It seems either really work well as an antidepressant, or not at all. I think that the serotonin-2 (5-HT2) blocking ability of the drug has a lot to do with it's ability to really screw-up some people. It's adverse actions in some people may have to do with the relative concentrations and locations of 5-HT2 receptors in these people.
>
> Perhaps the "fogginess" that you experienced had something to do with Serzone's action in the reticular activating system (RAS); the part of the brain responsible for the sleep/wake mechanisms of the body. The RAS contains the raphe nuclei, which is the part of the brain with the densest concentration of serotonin receptors, so this might be the reason why Serzone works so well in improving "sleep architecture" (ie. Serzone supposedly "normalizes" the different stages of sleep). Perhaps the blocking of certain serotonin receptor subtypes in this area buggering up your sleep/wake cycle and the fogginess might be due to your brain being stuck in one of the stages of sleep, while you are awake (caveat - this is just me thinking out loud, and is a total guess on my part).
>
> Serzone is a very potent inhibitor of CYP-3A3 and CYP-3A4 (which are closely linked), but it also inhibits, to a lesser extent, CYP-2D6 and CYP-1A2. Therefore it has the potential to increase plasma concentration of an incredibly wide range of medications, including caffeine. As for affecting herbs, the only one that I can think of affecting, off of the top of my head, is St.John's Wort.
>
> The incidence of contracting tardive dyskinesia (TD) from Zyprexa™ (olanzapine) is very low, probably due to it's "tweaking" of the dopamine-2 (D2) receptor (rather than binding irreversibly to it, like the traditional antipsychotics do). Risperdal™ (risperidone), at higher doses ( >6mg/day) causes EPS, because it seems to bind tighter (although still less than most traditonals) to D2 receptors, and doses over 6mg/day seems to saturate D2 receptors in the basal ganglia more so than other atypicals
>
> Also, I think that quite a few of the cases of TD reported to be caused by Zyprexa were, in actuality, the "unmasking" of TD caused by past traditional antipsychotic use. In some cases, traditional antipsychotics and anticholinergics (like Cogentin™ - benztropine) seem to hide the TD. Once these suseptible people switch to Zyprexa, the TD emerges. Again, I have no proof of this, other than what I have seen clinically. I was looking after one gentleman who had some mild signs of TD while taking Orap™ (pimozide) and Artane™ (trihexyphendyl). and when he was switched to Zyprexa, the TD came out with a vengence (ie. his tongue started flicking in and out of his mouth rapidly, all day, every day, while awake. In itself, Zyprexa seems not to cause TD very often at all.
>
> Again, this post is full of guesses and musings, but no real, proven hard facts. - Cam
Cam,This is a long post, but I really hope I can
get some feedback from you on your thoughts.
I *really* appreciate your insight.So here it goes:
I have found an interesting property of the zyprexa,
which is it "passes" both what I call "The Wellbutrin challenge"
and the "Lamictal challenge". The challenge is
to see if adminsitering the med at certain
levels hits the "snag". The "snag" is
pain in my head (jaw tension + tension headaches
and pressure in head) and numbs my emotions.Basically, I found that 4 anti-depressants
were therapeutic for me but all run into
the "snag" after a short while after
the depression relief.These were the meds, they all were taking
by themselves:
-St. John's Wort (at 1800 MG day)I actually felt best on this believe it or
not, and the effect lasted the longist without
manic symptoms.But, eventually I hit the "snag"
commentary:I think the NIMH test used 900 MG
which is too low for major depression.
Probably secretly funded by the pharmaceutical
companies to get bad results. Conspiracy Theory.- Wellbutrin. I tried this 3 times. It drove me
severly manic on 1st try, hypomanic on 2nd
try, and nada on the third try. The med would
wear off and hit the "snag"- Zoloft: immediate numbed my emotions, after one week
drove me hypomanic (my emotions returned briefly)
which wore off and it the "snag".- Lamictal. This one is weird. When I started
it at a low dose (~20 mg), I got a brief
relief of the pain and depression, that wore
of but I didn't hit the "snag". I increased
the dose to 150-225 mg, and it lifted my
major depression without hitting the snag.
I still had residual dysthymia at that dose.
When I bump Lamictal to 300 mg. I hit the
"snag". Strange....eventually the snag became a permanent
part of my life (after Zoloft) even without meds.
I don't have the emotional numbing when not on meds, just
the head pain. Klonopin releaves the "snag",
as well as Serzone,really high dose of
dyphenhyramine, and a moderate dose of cough
medicine xxx-dm. The dyphenhydramine and
dxm were found by accident. Adderall also
releives the pain when it works (I grow tolerant
really fast).
So after this I stayed at lower dose of Lamictal
and experimented with add ons.- Wellbutrin add on.I found that taking even 100 mg
Wellbutrin would severely exacerbate the "snag"
immediately with emotional numbing.
- St. John's wort. Same as Wellbutrin.
- Lamictal at 300 mg. Same as above.So my "challenge" is to see if any of the
three above add ones to Lamictal, or increasing
Lamictal dose *doesnt* hit the snag.
Well, guess what, I tried the
challenge with Wellbutrin and Lamictal and
I don't hit the snag while taking Zyprexa.I have a hypothesis to what is happening, but
it is lenghy do discuss.So my question is:
Should I bump the Lamictal dose to 300 mg and
leave the zyprexa alone, which is moderately helping
at 5 mg? I ask this because I am paranoid
about TD and I'm getting exacerbated
twitches on my face (not the snag, just benign
twitches).I have a list of other meds that dont hit
the "snag" but don't relieve the depression either.My theory on the "snag" is that I have a
hypo-dopaminergic state stemming
from the mesocortical track to the prefrontal
cortex where the facial mucles are and use
dopamine to tame acetylcholine.
A hypo-dopaminergic state into the frontal cortex
may explain the severe emotional numbing.
Almost like a negative psychosis.Thanks for any insight, I really appreciate it.
John
Posted by NikkiT2 on October 17, 2001, at 12:43:26
In reply to Re: zyprexa dose, posted by Cam W. on October 17, 2001, at 2:33:22
After experienceing annoying TD symptoms on many other AP's, I have found that Zyprexa really doesn't cause any.
I did, a few weeks ago, stupidly take an over dose of them.. i took 27 2.5mg tablets. I was up all night with leg shakes like I had never experienced. Not nice.
I hope this gives you some useful info.
Nikki xx
Posted by Collete on October 17, 2001, at 13:03:48
In reply to Re: zyprexa dose - TD, posted by NikkiT2 on October 17, 2001, at 12:43:26
> After experienceing annoying TD symptoms on many other AP's, I have found that Zyprexa really doesn't cause any.
>
> I did, a few weeks ago, stupidly take an over dose of them.. i took 27 2.5mg tablets. I was up all night with leg shakes like I had never experienced. Not nice.
>
> I hope this gives you some useful info.
> Nikki xxWhy did you take 27 pills? What is your usual dose?
Posted by NikkiT2 on October 17, 2001, at 15:43:13
In reply to Re: zyprexa dose - TD » NikkiT2, posted by Collete on October 17, 2001, at 13:03:48
It was just a very bad night.. It was a stupid stupid thing to do..
Mt usual dose os 3 x 2.5mg
Nikki x
> > After experienceing annoying TD symptoms on many other AP's, I have found that Zyprexa really doesn't cause any.
> >
> > I did, a few weeks ago, stupidly take an over dose of them.. i took 27 2.5mg tablets. I was up all night with leg shakes like I had never experienced. Not nice.
> >
> > I hope this gives you some useful info.
> > Nikki xx
>
> Why did you take 27 pills? What is your usual dose?
Posted by nathan on October 22, 2001, at 20:44:19
In reply to Re: zyprexa dose - TD » Collete, posted by NikkiT2 on October 17, 2001, at 15:43:13
Can you cut 5mg Zyprexa pills in half?
> It was just a very bad night.. It was a stupid stupid thing to do..
>
> Mt usual dose os 3 x 2.5mg
>
> Nikki x
>
> > > After experienceing annoying TD symptoms on many other AP's, I have found that Zyprexa really doesn't cause any.
> > >
> > > I did, a few weeks ago, stupidly take an over dose of them.. i took 27 2.5mg tablets. I was up all night with leg shakes like I had never experienced. Not nice.
> > >
> > > I hope this gives you some useful info.
> > > Nikki xx
> >
> > Why did you take 27 pills? What is your usual dose?
Posted by Cam W. on October 22, 2001, at 23:39:00
In reply to Re: zyprexa dose - TD, posted by nathan on October 22, 2001, at 20:44:19
> Can you cut 5mg Zyprexa pills in half?
Nathan - Yes, you can cut Zyprexa in half, but they have to be used within 7 days of doing so or they lose their potency. Also, don't get any of the powder in your eyes (it hurts like hell!). - Cam
Posted by Collete on October 23, 2001, at 8:34:44
In reply to Re: zyprexa dose - TD » nathan, posted by Cam W. on October 22, 2001, at 23:39:00
> > Can you cut 5mg Zyprexa pills in half?
>
> Nathan - Yes, you can cut Zyprexa in half, but they have to be used within 7 days of doing so or they lose their potency. Also, don't get any of the powder in your eyes (it hurts like hell!). - CamZyprexa was the most awesome med I ever took and I am so disappointed that I am one of those who developed a voracious appetitite and gained weight very quickly. Is there any posibility that taking 1/2 a pill could still work for me and perhaps not be as much of an appetite stimulant?
Thank you for being here! Collette
Posted by nathan on October 23, 2001, at 13:08:37
In reply to Re: zyprexa dose - TD » nathan, posted by Cam W. on October 22, 2001, at 23:39:00
I tried Zyprexa last night. I took 2.5 mg at 9:00pm. I am also on 25 mg of Zoloft. I slept great, but today I feel dopey and I have headaches. Is this normal? Does it go away?
> > Can you cut 5mg Zyprexa pills in half?
>
> Nathan - Yes, you can cut Zyprexa in half, but they have to be used within 7 days of doing so or they lose their potency. Also, don't get any of the powder in your eyes (it hurts like hell!). - Cam
Posted by Cam W. on October 23, 2001, at 23:58:12
In reply to CAM - a question about 1.25 mg Zyprexa » Cam W., posted by Collete on October 23, 2001, at 8:34:44
Collette - I have found that dose really doesn't have all that much to do with appetite. I have heard some people say that they were more hungry going from 5mg to 10mg, but not many. People gain on 2.5mg or 20mg and they seem to gain weight equally (I followed on lady who hadn't gained much weight on 35mg/day). I think you'd have more problems if the 1.25mg wasn't enough for therapeutic effect. - Cam
Posted by Cam W. on October 24, 2001, at 0:01:00
In reply to Re: zyprexa dose - TD, posted by nathan on October 23, 2001, at 13:08:37
> I tried Zyprexa last night. I took 2.5 mg at 9:00pm. I am also on 25 mg of Zoloft. I slept great, but today I feel dopey and I have headaches. Is this normal? Does it go away?
Nathan - The dopeyness and headache are start-up side effects. They usually fade by 2 weeks. - Cam
This is the end of the thread.
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