![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 1 to 10 of 10. This is the beginning of the thread.
Posted by OldSchool on March 13, 2002, at 20:41:07
The American Journal of Psychiatry
Copyright © 1999 American Psychiatric Association.--------------------------------------------------------------------------------
Volume 156(5) May 1999 pp 796-797
--------------------------------------------------------------------------------Tardive Dyskinesia With Quetiapine
[Letters To The Editor]
GHELBER, DIANA MD; BELMAKER, R.H. MDBeersheva, Israel.
--------------------------------------------------------------------------------
History...
Tardive Dyskinesia With Q...
Outline
REFERENCES
--------------------------------------------------------------------------------TO THE EDITOR: The new atypical antipsychotics have few extrapyramidal side effects and hold the promise of possible partial or total reduction of the risk of tardive dyskinesia. Only long-term studies will gauge the fulfillment of this promise. Clozapine rarely causes tardive dyskinesia [1]. Quetiapine, a new atypical antipsychotic with few extrapyramidal side effects, has not yet been reported to cause tardive dyskinesia. We report a case of tardive dyskinesia with quetiapine.
"Ms. A, a 44-year-old woman with schizophrenia and chronic active psychosis, was resistant to conventional antipsychotic therapy. She was treated for many years with clotiapine, haloperidol, perphenazine, thioridazine, and penfluridol. Most of these treatments were associated with severe akathisia and parkinsonism. Ms. A requested hospitalization to protect herself from imperative, frightening voices. She reacted in a bizarre manner to these voices and had paranoid delusions. During the years of her illness, she ceased working and extremely neglected her family and herself. On a regimen of quetiapine for 6 months, Ms. A completely recovered from her psychotic features and negative signs. Ms. A was first treated with a dose of 300 mg/day, but because of a strong sedative effect, the dose of quetiapine was reduced to 150 mg/day. Ms. A returned to her role as homemaker and renewed the social connections that she had ceased many years ago. Six months after beginning the treatment with quetiapine, involuntary choreiform movements of the tongue and jaw appeared, and a few weeks later, involuntary movements of the fingers appeared. Tardive dyskinesia was diagnosed. The involuntary movements persisted after the cessation of quetiapine. Unfortunately, after treatment with quetiapine was stopped, Ms. A relapsed into a severe psychotic episode. Treatment with clozapine then brought about an improvement in both her mental status and tardive dyskinesia."
This case suggests that quetiapine can cause tardive dyskinesia, although the frequency of its appearance is unknown and may be much rarer than with conventional neuroleptics. As with cases in the literature of clozapine-induced tardive dyskinesia [1], it is possible that the present case of tardive dyskinesia was due to the late effects of previous classical neuroleptic treatment.
DIANA GHELBER, M.D.
Posted by fachad on March 15, 2002, at 7:58:09
In reply to A case of Seroquel induced TD, posted by OldSchool on March 13, 2002, at 20:41:07
Thanks, Old School.
I've considered Seroquel for my Insomnia, but I had a pdoc for a long time that was just ADAMANTLY against anyone who was not in severe florid psychosis taking any antipsycotics.
He even cautioned me against amoxapine (an AD related to an AP) and compazine (an anti-nausea med related to an AP).
I don't know what happened in his practice or personal life that made him so cautious, I know he had many psychotic patients on them, but it has left me with a real aversion to APs and a healthy respect for the possibility of TD and EPS.
Posted by OldSchool on March 15, 2002, at 10:30:35
In reply to Re: A case of Seroquel induced TD » OldSchool, posted by fachad on March 15, 2002, at 7:58:09
> Thanks, Old School.
>
> I've considered Seroquel for my Insomnia, but I had a pdoc for a long time that was just ADAMANTLY against anyone who was not in severe florid psychosis taking any antipsycotics.Your Pdoc is a smart man. You should never take atypical anti-psychotics for "insomnia." Its simply not worth the risk.
>
> He even cautioned me against amoxapine (an AD related to an AP) and compazine (an anti-nausea med related to an AP).
I would never take amoxapine that is a tricyclic with a built in old style anti-psychotic...you are asking for TD or EPS with that drug.>
> I don't know what happened in his practice or personal life that made him so cautious, I know he had many psychotic patients on them, but it has left me with a real aversion to APs and a healthy respect for the possibility of TD and EPS.Maybe he has seen the neurological damage done by anti-psychotics and simply doesnt want you to experience that sort of thing.
Old School
Posted by crepuscular on March 15, 2002, at 11:00:27
In reply to Re: A case of Seroquel induced TD, posted by OldSchool on March 15, 2002, at 10:30:35
i'm not sure the real-world data on Seroquel (in particular) justify the kind of fear you folks are talking about; the case presented is complex and unclear. but seroquel is probably is overkill for insomnia or simple anxiety.
on the other hand, "insomnia" for me is often the beginning of the manic/hypomanic process. regular sleep is restorative & protective against future attacks for me. i can also take effective doses of antidepressants while on seroquel.
it's the old cost-benefit analysis i guess, subjectively mediated by symptom severity & the experience of your doc...
Posted by SLS on March 15, 2002, at 18:09:38
In reply to Re: A case of Seroquel induced TD, posted by OldSchool on March 15, 2002, at 10:30:35
Hi OldSchool.
> "Ms. A, a 44-year-old woman with schizophrenia and chronic active psychosis, was resistant to conventional antipsychotic therapy. She was treated for many years with clotiapine, haloperidol, perphenazine, thioridazine, and penfluridol."
It is possible that the true culprit was this person's prior exposure to the older neuroleptics. Although I don't know exactly how it happens, Seroquel (quetiapine) may have "unmasked" the TD that had been both produced *and* masked by the likes of Haldol.
> "As with cases in the literature of clozapine-induced tardive dyskinesia [1], it is possible that the present case of tardive dyskinesia was due to the late effects of previous classical neuroleptic treatment"
I am not touting the safety of using Seroquel or any of the other atypical neuroleptics, but a fuller understanding of the risks these drugs carry of producing TD must take into consideration the treatment history of those people in whom it emerges. Perhaps like Cam W. could provide some insight into the case report. I don't know how to account for the 6 month period of latency between the introduction of Seroquel and the appearance of TD. Perhaps Seroquel is the culprit, but I don't think this case can segregate the contributions of all of the drugs involved. On Medline, you will find anecdotal reports of EPS, including TD, observed in association with all of the atypical neuroleptics. It would be interesting to compare the treatment histories of the individual cases.
Of the atypicals, it is suggested that Clozaril (clozepine) and Seroquel are the least apt to produce EPS. Risperdal seems to be the most apt. In fact, Clozaril and Zyprexa are sometimes used to mitigate pre-existing EPS. It is thought that the ability of these drugs to block serotonin 5-HT2a/c receptors yields a better balance between serotonin and dopamine pathways. Some researchers hypothesize that this balance helps protect one from developing TD. However, Seroquel is the weakest antagonist at these receptors. It is also the weakest dopamine D2 antagonist of all the neuroleptic antipsychotics. Because Haldol and the other older neuroleptics bind so tightly to the D2 receptor, any AP-induced D2 receptor supersensitivity would be masked because most of them remain occupied and blocked by these same drugs. Being the weakest D2 antagonist, and without sufficient 5-HT2a/c receptor antagonism to promote a balance, Seroquel would be the least capable of maintaining the mask, thus allowing EPS to bleed through.
To examine the relative potency of these drugs to bind to various receptors, you can take a look at the following chart. It is an inverse association. The bigger the number, the weaker the attachment.
http://sl.schofield3.home.att.net/medicine/aripiprazole_binding.pdf
- Scott
Posted by OldSchool on March 15, 2002, at 19:00:20
In reply to Re: A case of Seroquel induced TD » OldSchool, posted by SLS on March 15, 2002, at 18:09:38
> Hi OldSchool.
>
> > "Ms. A, a 44-year-old woman with schizophrenia and chronic active psychosis, was resistant to conventional antipsychotic therapy. She was treated for many years with clotiapine, haloperidol, perphenazine, thioridazine, and penfluridol."
>
> It is possible that the true culprit was this person's prior exposure to the older neuroleptics. Although I don't know exactly how it happens, Seroquel (quetiapine) may have "unmasked" the TD that had been both produced *and* masked by the likes of Haldol.
>
> > "As with cases in the literature of clozapine-induced tardive dyskinesia [1], it is possible that the present case of tardive dyskinesia was due to the late effects of previous classical neuroleptic treatment"
>
> I am not touting the safety of using Seroquel or any of the other atypical neuroleptics, but a fuller understanding of the risks these drugs carry of producing TD must take into consideration the treatment history of those people in whom it emerges. Perhaps like Cam W. could provide some insight into the case report. I don't know how to account for the 6 month period of latency between the introduction of Seroquel and the appearance of TD. Perhaps Seroquel is the culprit, but I don't think this case can segregate the contributions of all of the drugs involved. On Medline, you will find anecdotal reports of EPS, including TD, observed in association with all of the atypical neuroleptics. It would be interesting to compare the treatment histories of the individual cases.
>
> Of the atypicals, it is suggested that Clozaril (clozepine) and Seroquel are the least apt to produce EPS. Risperdal seems to be the most apt. In fact, Clozaril and Zyprexa are sometimes used to mitigate pre-existing EPS. It is thought that the ability of these drugs to block serotonin 5-HT2a/c receptors yields a better balance between serotonin and dopamine pathways. Some researchers hypothesize that this balance helps protect one from developing TD. However, Seroquel is the weakest antagonist at these receptors. It is also the weakest dopamine D2 antagonist of all the neuroleptic antipsychotics. Because Haldol and the other older neuroleptics bind so tightly to the D2 receptor, any AP-induced D2 receptor supersensitivity would be masked because most of them remain occupied and blocked by these same drugs. Being the weakest D2 antagonist, and without sufficient 5-HT2a/c receptor antagonism to promote a balance, Seroquel would be the least capable of maintaining the mask, thus allowing EPS to bleed through.
>
> To examine the relative potency of these drugs to bind to various receptors, you can take a look at the following chart. It is an inverse association. The bigger the number, the weaker the attachment.
>
> http://sl.schofield3.home.att.net/medicine/aripiprazole_binding.pdf
>
>
> - Scott
Scott, I dont exactly agree with your ideas about atypicals and EPS. The bottom line is that ANY anti-psychotic can produce EPS. Even Clozapine. While it may or may not be true that atypicals are safer than typicals, atypicals are still not exactly the safest drugs in the world to take. I believe this is especially true if you are not floridly psychotic, as in schizophrenic or manic psychotic. I dont care if it is a "weak D2 binder" or whatever. If the drug antagonizes d2 receptors it can cause EPS...period.All anti-psychotics can cause these problems. The drug companies claim "their atypical is safest" 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. EPS being defined as:
1) numb tongue
2) tight throat
3) tight, contracted muscles (legs, arms, chest, back)
4) muscle pops and twitches
5) tight, contracted feeling on the back of head.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.
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.
Hell its even being admitted by mainstream psychiatry that plain old SSRIs can cause EPS in a minority of people taking them. I just posted an article several times on here about SSRI induced movement disorders and its from a credible psychiatry source online, not some anti-psychiatry website.
If you give atypicals to someone who is depressed or anxious but not floridly psychotic, the odds are they do not have the high dopamine levels schizophrenics and manic depressives usually have. This means that even small amounts of dopamine receptor antagonism can cause neurological damage. You have less leeway with dopamine if you are just depressed or anxious, but not psychotic in the classic, schizophrenic sense.
Can the BS...all atypical anti-psychotics can cause EPS equally. 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.
Finally, the best way to get rid of EPS is bilateral ECT.
Old School
Posted by SLS on March 16, 2002, at 9:11:01
In reply to Re: A case of Seroquel induced TD, posted by OldSchool on March 15, 2002, at 19:00:20
Hi OS.
> Scott, I don't exactly agree with your ideas about atypicals and EPS. The bottom line is that ANY anti-psychotic can produce EPS. Even Clozapine.
I think we are in complete agreement here with regard to those drugs that are currently marketed.
> While it may or may not be true that atypicals are safer than typicals, atypicals are still not exactly the safest drugs in the world to take.
Neither is penicillin.
> I believe this is especially true if you are not floridly psychotic, as in schizophrenic or manic psychotic. I don't care if it is a "weak D2 binder" or whatever. If the drug antagonizes d2 receptors it can cause EPS...period.
Well, I would not feel comfortable making such a statement. Some neuroleptic antipsychotics are selective as to which regions of the brain they act. For example, aripiprazole (Abilitat) blocks D2 receptors in areas of the brain suspected to be involved in schizophrenia (prefrontal cortex), but not in those regions involved with movement, i.e. nigrostriatal dopamine pathways. In addition, some of the newer drugs being investigated bind to D2 receptors, but only momentarily. They hop-on and then hop-off. It is thought that perhaps no one receptor "believes" it is being blocked, although it is sure that it is not being stimulated. If the receptor doesn't perceive a change in its environment or function, it doesn't send a message to the neuron's nucleus asking it to synthesize more receptors.
> All anti-psychotics can cause these problems.
So far, it looks that way.
> The drug companies claim "their atypical is safest"
Surely, one of them must be.
I don't know if any drug company claims that their neuroleptic antipsychotics are without the risk of producing EPS. I'm pretty sure that none do. Each neuroleptic is distributed with an FDA-approved pamphlet known as a package insert or label. Every bottle. I'm sure your pharmacist will give you one if you ask. It would be quicker, though, to look through the Physician's Desk Reference (PDR), in which you will find for each drug a reproduction of the information found on the package insert. To the best of my knowledge, they all state in black-and-white the percentage of subjects that developed EPS while taking the drug.
> 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.
> 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.
> 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.
> 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?
Risk versus benefit.
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.
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?
> 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
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.
>
> 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
Posted by crepuscular on March 16, 2002, at 14:27:23
In reply to Re: A case of Seroquel induced TD, posted by OldSchool on March 16, 2002, at 13:30:38
lifetime risk (untreated) of suicide for me >= 50%. probability of work disability from extreme mood cycling & depression = 100%. risk of losing important relationships & insulting those around me when manic = 100%. risk of massive insomnia=100%. probability that an AD will give me hypomania within 2 months >=90%.
ability to make sustained progress on artistic projects and personal relationships when treated = 100%. ability untreated <= 25%.
this is the real-world context of risk from neuroleptic drugs for me. yes, i could be one of the proportionally few people who get TD or NMS. but having tried lots of things, and even *losing* weight on seroquel(!), i have to say i'm mostly thankful for it being there.
someday there will be actual curative treatment - without risk -for major affective disorders. but we are simply not there yet.
Posted by SLS on March 17, 2002, at 22:46:50
In reply to Re: A case of Seroquel induced TD, posted by OldSchool on March 16, 2002, at 13:30:38
Hi OldSchool.
Thanks for the URL. Pretty hefty.
> 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.
Do you think the Risperdal was responsible for your diminished response? It made me feel fatigued and depressed the first time I took it, but I was in a mixed-state mania at the time. On a similar note - this really sucks, you know?
> 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'm still curious, have you ever taken one of the older APs?
I don't know if this applies to you, but Tegretol is sometimes used to treat aggressive conditions. Perhaps Trileptal is similarly effective.
> 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.
I wasn't real happy with Seroquel either. I felt irritable and bitchy.
> 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.
Your instincts are good. It turns out that the incidence of neuroleptic-induced EPS is higher for someone being treated for bipolar disorder than it is for schizophrenia.
> The drugs actually raise blood sugar levels Scott, I read that specifically.
There are some pretty compelling anecdotal reports implicating clozapine and olanzapine with de novo diabetes and other disturbances in glucose / insulin / triglyceride dynamics. I have a hard time believing that they are all secondary to weight-gain, especially when it is reported that these conditions resolve so immediately upon drug-discontinuation. If I end up on Zyprexa, I plan to take blood-tests from time to time. I have a family history of diabetes II on both sides.
> First of all, I dont agree with your penicillin analogy.
Why not?
> I think penicillin is a way safer drug to take than anti-psychotics.
Not for those who have died from anaphylactic shock.
> Secondly, the question about whether you should try SSRIs being that you are bipolar, I just dont know.
The point I was trying to make is that very few drugs are without a liability to produce side effects. Since you mentioned the liability of SSRIs to produce EPS, I was curious if you thought treating a "simple" depression (as opposed to schizophrenia) with a drug that produces EPS can be justified. I know that's a rhetorical question, but I think it demonstrates the difficulties found in the decision-making process involved in treating illness in general. I'm a pretty naive fellow, so I can't help but to believe that drug companies are not acting in collusion to poison us. I still like to think that some of their R&D people give a damn. In the absence of collusion, I think capitalism demands it. (If there is one thing less productive than being young and idealistic, it is being old and idealistic). :-)
I find your posts informative and valuable. Thanks.
- Scott
This is the end of the thread.
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