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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 12 of 12. This is the beginning of the thread.
Posted by Shelley on August 29, 2001, at 14:44:26
Are people with a history of taking neuroleptics at increased risk for developing Parkinson's Disease (not drug-induced parkinsonism) in the future?
And- does anyone know of any effective treatment for tardive dyskinesia?
Thanks.
Posted by SalArmy4me on August 29, 2001, at 15:44:46
In reply to neuroleptics , posted by Shelley on August 29, 2001, at 14:44:26
http://www.vh.org/Providers/Conferences/CPS/08.html
Abstract: Year Book of Psychiatry and Applied Mental Health Volume 1999(8) Annual 1999 pp 385-386. Treatment of Tardive Dyskinesia:
"Introduction.-The introduction of clozapine and other atypical antipsychotic agents has raised hopes that tardive dyskinesia (TD) may be eradicated someday. For now, this disorder remains a significant clinical problem for patients and physicians. Management approaches to TD are described.
Managing TD.-Most TD is mild. Therapeutic efforts focus on minimizing neuroleptic exposure or changing treatment to atypical agents in patients with mild to moderate TD. Tardive dyskinesia typically does not progress, which indicates that the risk of remaining on typical neuroleptics is slight. Moderate to severe TD is more challenging, and patients typically require medication to suppress symptoms Table 4. Most suppressive agents have limited success. No treatment strategy is clearly superior or even successful in most patients. Raising the doses of typical neuroleptics may be useful for short-term suppression, yet the long-term efficacy and risk of this approach have not been clearly elucidated. Data on atypical neuroleptics are sparse. Clozapine has a short-term suppressive effect that is weak, but patients may experience improvement with long-term treatment.
Other Approaches.-Other medications that have relatively few side effects and may have suppressive properties include calcium blockers, adrenergic antagonists, and vitamin E. Gamma-amino-butyric acid agonists agents and dopamine can be helpful but are accompanied by troubling side effects. Anticholinergic agents and botulism toxin have also been effective in treating TD.
Conclusion.-Despite the new generation of neuroleptics, TD remains a challenging clinical problem. A better understanding of the mechanisms of actions of atypical neuroleptics and of the physiology of the basal ganglia should enhance treatment approaches.
[r tri, filled] This article was completed by a research team who is well known in the area of antipsychotic medication treatment. This thorough review covers the waterfront of the various options available to us and presents a thoughtful flow diagram (untested) that is useful for clinicians. The authors end with the hope that the newer agents that appear to have a lower risk for development of tardive dyskinesia may provide a brighter future for patients who require treatment with antipsychotics. The article itself is certainly well worth reading, with a take-home message (see table) which will probably be useful to many busy clinicians."
R.B. Lydiard, Ph.D., M.D.
Professor of Psychiatry and Behavioral Sciences, Medical University of South Carolina; Director, Clinical Psychopharmacology Research Division, Institute of Psychiatry, Medical University of South Carolina, Charleston, South Carolina.
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The Salvation Army Life Service Conference 2001: Heart to God, Hand to Man.
Posted by Shelley on August 29, 2001, at 16:12:15
In reply to Re: neuroleptics , posted by SalArmy4me on August 29, 2001, at 15:44:46
Thank you very much for your links on TD and expired meds :)
Posted by Cam W. on August 29, 2001, at 17:36:38
In reply to neuroleptics , posted by Shelley on August 29, 2001, at 14:44:26
Shelley - The only treatment that I have seen work, with any sort of sustained efficacy for TD, was Clozaril™ (clozapine). The problem with using this med is it's profound side effects, and pain-in-the-ass weekly/biweekly blood monitoring. Another discoraging thing is that one may not see significant improvement for 8 to 12 months.
The good side to all this is that when a result is seen, it is usually dramatic. The TD becomes hardly noticeable unless you are looking for it very closely (ie. when it works, it works like a damn). If one's doctor does decide to use Clozaril to treat tardive dyskinesia, one has to remember that it is not going to be effective immediately.
I hope that this is of some help. - Cam
Posted by judy1 on August 29, 2001, at 19:36:49
In reply to neuroleptics , posted by Shelley on August 29, 2001, at 14:44:26
Shelli,
So far I've had little luck resolving my TD (although I haven't tried Cam's protocol- mainly out of fear). Cogentin did seem to lessen my hand tremor. I think the biggest problem is I still need neuroleptics occasionally with manic episodes- and then my symptoms worsen again. I hope you're not experiencing any symptoms. I don't know about an increased risk for Parkinsons- sorry. My pdoc is convinced time is the biggest factor in improvement, and I think he may be right. Take care, judy
Posted by Shelley on August 30, 2001, at 3:09:10
In reply to neuroleptics , posted by Shelley on August 29, 2001, at 14:44:26
Posted by Duda on August 30, 2001, at 16:07:12
In reply to Cam and Judy- thank you both :) (nm), posted by Shelley on August 30, 2001, at 3:09:10
I've been operating on the understanding that the risk of TD or EPS is all but eliminated by using atypical APs, especially if used in an AD capacity.
I myself am starting to take a 50 mg. dose of Amisulpride, and want to be sure I haven't been lulled into not fearing a legitimate concern.
Posted by Cam W. on August 30, 2001, at 16:26:42
In reply to Cam et al...., posted by Duda on August 30, 2001, at 16:07:12
Duda - The incidence of TD with the newer atypical antipsychotics (aAps) seems to be very small. This is probably because the aAPs do not irreversibly bind to dopamine receptors like the older antipsychotics do. Thus the dopamine receptors can still bind dopamine, as well as th aAP. This is especially important in the extrapyramidal system, where the loss of dopamine binding is thought to cause EPS and TD.
This said, there have been instances of EPS and TD with all of the aAPs. The problem with determining if the aAP is the causative factor is debatable. Most of the people who get TD with the aAPs have taken traditional antipsychotics in the past, and it has been suggested that the aAPs just unmask latent TD, which could have been caused by the older medication.
Theoretically, even if one hadn't taken traditional antipsychotics, one could still get TD, depending on the concentration of dopamine receptors in the extrapyramidal system. This dopamine receptor concentration would probably be determined by genetics.
In any case, the incidence of TD from aAPs is very, very low, when compared to the older agents. One should not be lulled into a false sense of security, but TD is unlikely to occur when taking aAPs. As a legimate concern, I wouldn't worry about it on a daily basis; it is not really that much of a concern.
I hope that this is not of some help. - Cam
Posted by JohnL on August 30, 2001, at 16:36:20
In reply to Cam et al...., posted by Duda on August 30, 2001, at 16:07:12
> I've been operating on the understanding that the risk of TD or EPS is all but eliminated by using atypical APs, especially if used in an AD capacity.
>
> I myself am starting to take a 50 mg. dose of Amisulpride, and want to be sure I haven't been lulled into not fearing a legitimate concern.Duda,
Where did you get your Amisulpride? I would love to find a new source for it.
Thanks,
John
Posted by Duda on August 30, 2001, at 16:56:12
In reply to Re: Duda Question, posted by JohnL on August 30, 2001, at 16:36:20
Cam...Thanks. You mentioned something about genetics. My Grandmother nearly died from NMS after a lifetime of typical APs. She is schizophrenic.
I am not (possibly schizoaffected, but generally prone to depression and anxiety), but there is that concern. Should I take extra precaution?
And John, I recently ordered my Amisulpride from MOPID, which is a source you may have given me.I changed my user name when I switched to a new computer. Also, this is a little more annonymous.
MOPID is kind of expensive, but they don't require a prescription, which my pdoc won't supply.
Sorry I couldn't be of more help.
Duda
Posted by Cam W. on August 30, 2001, at 17:37:33
In reply to Re: Duda Question » JohnL, posted by Duda on August 30, 2001, at 16:56:12
Duda - With a genetic history of NMS in your family, I would definitely recommend that you have a doctor follow your progress. A doc can watch for early warning signs of EPS, TD, and NMS, that you may not notice yourself. - Cam
Posted by Sunnely on August 31, 2001, at 19:12:39
In reply to Re: Duda Question » JohnL, posted by Duda on August 30, 2001, at 16:56:12
> Cam...Thanks. You mentioned something about genetics. My Grandmother nearly died from NMS after a lifetime of typical APs. She is schizophrenic.
> Should I take extra precaution?
As Cam mentioned above, a family history of NMS (neuroleptic malignant syndrome) puts you at higher risk for NMS. But this risk alone is probably not enough to cause NMS as it usually occurs due to a combination of factors. Not everyone who has a family history of NMS will develop it when treated with a neuroleptic (antipsychotics). There were also patients who developed NMS from one particular neuroleptic and were successfully re-challenged with another neuroleptic or even same neuroleptic. Although neuroleptics have been commonly implicated, other non-neuroleptics have been found to be the culprits. For example, metoclopramide (Reglan) has been reported to induce NMS; abrupt discontinuation of antiparkinsonian drugs such as levodopa also reported to induce NMS; abrupt discontinuation of anticholinergic drug also implicated.
The risk of NMS in someone on neuroleptic rises if the following conditions are concomitantly present dehydration, agitation, mood disorders, brain damage, withdrawal states, use of rapid dose titration (escalation) and use of intramuscular injections.
Virtually all antipsychotics (old and new) have been reported to cause NMS.
For more info on NMS, go to:
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