Posted by OldSchool on March 16, 2002, at 13:30:38
In reply to Re: A case of Seroquel induced TD » OldSchool, posted by SLS on March 16, 2002, at 9:11:01
> > but in the end its all BS because all of them can cause EPS and even TD. Ive tried Zyprexa, Risperdal and Seroquel all at low doses and everyone of them gave me EPS equally.
>
> Unfortunately, you are not alone. There are a bunch of people here who are equally prone to the development of EPS when using low dosages of atypical neuroleptics.
>
> I am curious though. I haven't followed your posts (nor anyone else's lately) so as to know what illness you are treating with antipsychotics. How long ago were you first treated with an antipsychotic? Which one(s)? I'm sure you understand the reason I ask this. If you were treated with one of the older typical neuroleptics prior to your exposure to the atypicals and prior to the the emergence of EPS, then your case could not be included in an investigation to examine the potential for any of the atypicals to produce EPS.Scott Ive been on low dose atypicals a few times in the last four years, added to whatever antidepressant I was on at the time. Initially plain old SSRIs activated really well for me, but after half a mg of Risperdal was added to my antidepressant for two months, my AD faded out on me and never really has activated good since. As for reasons why Ive been on low dose atypicals a few times, I was on them because I was a crazed lunatic with severe depression.
I was put on atypicals because I have a "gruff" personality" I was told repeatedly and a few of my psychiatrists were scared of me I think, thought I was maybe a psycho. Basically I was put on them cause Im kind of mean. Agitated depression, whatever you want to call it. I tried half a mg Risperdal, 2.5 mg Zyprexa and 50 mg Seroquel at various times. Actually I went up to 100 mg Seroquel on my own once and when I did that my personality went very "flat" and I felt like a robot.> > Every atypical I have tried gave me these symptoms. I dont believe these BS claims that atypical anti-psychotics are safe.
>
> > Because I dont believe they are safe.
>
> Safe. Safer. Safest.
>
> The latter two words can be established through observation, since the drugs being compared represent a frame of reference. The first word is a judgment. What are the parameters you use to judge drugs as being safe or unsafe? I'm not sure I would judge these drugs as being safe. I am a bit afraid of them. However, many doctors with years of real-life experience treating real-life people do judge them as being safe - safe enough to justify their use.
>I think they are safer if you are schizophrenic and have high levels of dopamine to begin with Scott. Thats what I personally believe. I might be wrong.
> > Plus on top of this all the atypicals are bad about raising blood sugar. Zyprexa has been implicated in quite a few cases of diabetes.
>
> This is true. Is their any clear evidence that the causation of these things are not secondary to the weight-gain these drugs produce? I don't know. If it is, then perhaps steps can be taken to avoid it.The drugs actually raise blood sugar levels Scott, I read that specifically. Add the weight gain and sitting around on your ass all the time drugged up and voila you have diabetes. Clozapine is real bad about that and so is Zyprexa. All the atypicals can cause raised blood sugar though.
>
> > Hell its even being admitted by mainstream psychiatry that plain old SSRIs can cause EPS in a minority of people taking them.
>
> Yeah, I was going to bring that up. I'm glad you did. Like I said, even penicillin is not without the risk of fatal reactions. I have been well aware of the risk of SSRI-induced EPS for a number of years, including the possible emergence of suicidality due to the induction of akathisia. It is my belief that Prozac has caused some people to commit suicide. Still, I might decide to start taking Celexa next month to treat a severe and treatment-resistent bipolar depression. Do you think I should? Are SSRIs safe? Are they safe enough for me to try?First of all, I dont agree with your penicillin analogy. I think penicillin is a way safer drug to take than anti-psychotics. Secondly, the question about whether you should try SSRIs being that you are bipolar,
I just dont know. Ask your doctor. Im not a doctor. I always read that Wellbutrin was the preferred antidepressant for bipolar. I always read and heard many bipolars cant tolerate SSRIs, especially without a mood stabiliser underneath.>
> Risk versus benefit.
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> Is there no degree of severity of illness for which it is worth the established and quantized risk to treat? I know a few schizophrenics and members of their immediate families whom think there is.I think for schizophrenics and some manic depressives these drugs are perfectly fine.
>
> What about depression? For me, I thought it was worth the risk. I've tried three so far. Unfortunately, though they produced an improvement of my depression, they also produced cognitive side effects that forced me to stop taking them.
>
> > Can the BS...all atypical anti-psychotics can cause EPS equally.
>
> How did you go about coming to this conclusion?Because all three of the atypicals I have tried have caused the same exact EPS symptoms in me Scott. I didnt find Seroquel caused EPS any less than Risperdal did, in fact I have had the worst EPS I ever had on Seroquel and unlike with Risperdal and Zyprexa, the EPS lasted AFTER I went off the Seroquel. In fact, thats when it really showed up bad...after I went off it.
I dont listen to all the drug company crap anymore. I think some of it is just plain BS. I think lawyers will have a field day when Eli Lilly gets Zyprexa augmentation of SSRIs FDA approved for non psychotic TRD. Wait until that happens and a bunch of unipolar depressed people who never hallucinated or had schizo symptoms start getting bad EPS and diabetes on Zyprexa. Id love to be the lawyer in on that...probably would get rich easy.>
> > Except for maybe Clozapine, which I have never taken and cannot discuss. I do know Clozapine is considered to be extremely safe when it comes to movement disorders, but Im skeptical of even that.
>
> I am glad to see that your judgment of clozapine is not without objectivity.
>
> > Finally, the best way to get rid of EPS is bilateral ECT.
>
> I didn't know that (no sarcasm). I'd like to know more about it.Scott, ECT has off label uses for treating both parkinsons disease and TD. EPS is very similar in some respects to parkinsons. When I went to my family doctor and got diagnosed with Seroquel induced EPS, he told me ECT would help both conditions. ECT increases dopamine levels. ECT has anti-parkinsons effects in addition to its well publicized anti-depressant qualities.
Go here to this link and scroll down to where it talks about using ECT for treating TD. Schizophrenics who have ECT in have lower rates of TD than do schizophrenics who dont do ECT.
http://www.acnp.org/g4/GN401000108/Default.htm
Movement Disorders
The potential for acute extrapyramidal syndromes, particularly neuroleptic-induced parkinsonism (NIP), and for persistent tardive dyskinesia are major drawbacks of traditional neuroleptic treatment. Although extrapyramidal symptoms are generally considered to be reversible, prospective studies have suggested that neuroleptic-induced parkinsonism may predict the subsequent development of tardive dyskinesia.
Because ECT is unique in having both antipsychotic and antiparkinsonian properties, it may exert ameliorative effects on neuroleptic-induced parkinsonism (1, 29, 19). For example, Goswami et al. (19) studied nine schizophrenic inpatients with a longitudinal triphasic design, first using neuroleptics, then neuroleptics and ECT, and then neuroleptics. Neuroleptic-induced parkinsonism was significantly reduced in stepwise fashion when patients were treated with ECT. Recently, Mukherjee and Debsikdar (35) introduced the notion that ECT may protect against the later development of neuroleptic-induced parkinsonism and tardive dyskinesia. They examined 35 DSM-IIIR schizophrenic patients who were on neuroleptics for at least 2 weeks, all of whom were receiving (n = 15) or had received (n = 20) a course of unmodified bilateral ECT during the index episode. None of the patients had bradykinesia, rigidity, or postural instability and only one patient met the research diagnostic criteria for probable tardive dyskinesia. Mukherjee and Debsikdar (35) speculated that if neuroleptic-induced parkinsonism is a risk factor in the development of tardive dyskinesia, ECT may ultimately protect against tardive dyskinesia by preventing initial neuroleptic-induced parkinsonism. At the neurophysiological level, there is evidence in rodents that electroconvulsive shock (ECS) prevents the development of dopamine receptor supersensitivity with exposure to dopamine antagonists (29) and results in increased D1 receptor density without impact on the D2 receptor density (16).
There are also suggestions that a history of ECT may be associated with a low prevalence or delayed development of tardive dyskinesia. Gardos et al. (18) evaluated 122 schizophrenic outpatients in Hungary and reported a striking absence of severe tardive dyskinesia. They suggested that the low prevalence was due to the use of ECT to treat exacerbations and the avoidance of high dosage neuroleptic treatment. In an American sample, Cole et al. (3) recently reported that a history of ECT was associated with a lower risk and delayed appearance of tardive dyskinesia. As noted, Mukherjee and Debsikdar (35) found virtually no tardive dyskinesia in an Indian sample, which they attributed to the use of ECT. Schwartz et al. (59), in an Israeli sample, reported a reduced incidence of tardive dyskinesia among male schizophrenic patients with a history of ECT. If, in fact, ECT does offer long-term protection against the iatrogenic effects of concurrent or later exposure to neuroleptics, this would also contradict the general impression that the behavioral and physiological effects of ECT are uniformly transient (50).
In both open and sham-controlled trials, ECT has been found to improve clinical symptoms in idiopathic Parkinson's disease, at least on a short-term basis (1, 2, 29). Typically, L-dopa requirements are sharply reduced when parkinsonian patients receive ECT. The persistence of the beneficial effects are unpredictable and highly variable. The utility of ECT as a long-term treatment for medication-resistant Parkinson's disease has yet to be tested, as use of maintenance ECT has not been evaluated.
Old School
poster:OldSchool
thread:97844
URL: http://www.dr-bob.org/babble/20020313/msgs/98308.html