![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 5974 to 5998 of 10407. Go back in thread:
Posted by Lyrical13 on January 2, 2004, at 5:31:48
In reply to re: atypical NMS, posted by maxx44 on January 1, 2004, at 19:34:37
OK Maxx...scary but worth checking out. Personally I think all meds should be titrated off slowly to avoid bad effects. But I still don't know what the initials NMS stand for. I know Seroquel is an atypical antipsychotic and they really don't know what long-term effects it will have because it is much newer than other meds. I'll check out "supersensitive psychosis". NMS=???????
Posted by helenag on January 2, 2004, at 17:03:15
In reply to Re: Effexor XR - Some Advice Desperately Needed.HELP., posted by joeyD on December 31, 2003, at 8:09:23
> Hey guys sorry about taking up time here. I hope I'm posting in the right place. I have a few questions. I have just started taking 75 mg of Effexor XR about a week ago for GAD and mild depression. Since I started I have not been able to sleep, however I have been able to function surprisingly well. As of last night I have been having some extreme OCD symptoms!! I could not even think about going to sleep last night so I took 1mg of Klonopin and when I woke up this morning the OCD is still here but even worse! Its driving me crazy! I never had these feelings before and its really bothering me. BTW, they are not dangerous in any way to others or myself. Could the Effexor be causing this? Also, does this med generally cause extreme aggitation? I've been getting angry extremely easilly for a few days now. Sorry to bother you guys about this stuff but my doctor wont talk to me over the phone and my appointing is not until another two weeks. And yes, I am currently looking for a new one.
>
> Thanks in advance!!
>
> JoeyJoey: Doesn't your pdoc have a nurse in the office that you can talk to??? Usually you can leave a message about meds with the nurse and she will talk to the doctor for you and call you back. Have you tried that?? If you just asked for the doctor without telling the office why, it is usually no wonder you wouldn't get a call back.
I find it very strange that you would receive no help with a med question or problem from a pdoc's office. Very strange. Try calling again and this time tell whomever answers the phone why you are calling (if you didn't before) and that you need someone to call you back asap. If you did do this and no one responded, try again. If you get the same result, it seems like this is quite an unusual office here.....hope you are feeling better soon. helen. and if you have no luck with this doctor, find a new one pdq!!!
Posted by maxx44 on January 2, 2004, at 18:18:18
In reply to re: atypical NMS, posted by Lyrical13 on January 2, 2004, at 5:31:48
search 'neuroleptic malignant syndrome' (NMS), and 'atypical NMS'---when drs. speak of any neuroleptic they use a phrase, 'dopamine and/or dopamine serotonin' BLOCKADE---this is a misnomer as these drugs don't 'block' anything, rather Demolish the deep-brain production facilities and receptors of these key elements of 'self'. that's why those having used benzos or worse, neuroleptics, usually long-term but often even briefly, suffer the fate of always needing the drug. their born 'hardware' has been 'wiped'. scary? please, don't kill the messenger, as many would.
Posted by Mercedes on January 2, 2004, at 21:28:06
In reply to Re: Anyone had success on Effexor XR? , posted by maxx44 on January 1, 2004, at 22:51:59
Geesh! you seem to have a negative response to everything. You respond and contradict others' 'good' or 'helpful' advice/intentions and manage to make everything so negative. This response and many you have posted are totally unacceptable, "killing of minds". Your opinion was not asked for. I know it's a 'free board' but for heaven's sake, don't scare people. We already have enough anxiety without having to hear our med's are "poisons".
If a person makes a comment on what med has worked for them, please don't say things like "death" or "letal". Like I said, we have enough anxiety/depression and don't need to hear sh*t like that. Keep those to yourself. IMHO
*************************************
> the rediculous killing of minds when not appropriate, rather money-driven', that bothers me. if you may control the drug and use infrequently as intended---3 cheers. inderal? why do you think so many pop music icons have died from heroin? same deal. super-anxiety relief. right? or so they claim. put me to sleep for 26 hours--scripted to lessen lithium/imipramine 'tremor'. i'd still watch it and use only when a known need is overpowering.
> it's like being a smoker---you'd best know cigs (a 'street-med as alcohol') or meds may be lethal and have 'cumulative' effects way down the line. if you close the deal, and infrequent inderal helps? great---start using it for every stressor, trouble you don't want to ever see, nor should you. IMHO.
Posted by Zellie on January 2, 2004, at 22:48:02
In reply to Re: Max, stop being so negative! » maxx44, posted by Mercedes on January 2, 2004, at 21:28:06
I, too, would like to see more encouraging talk here. Yes, we all have concerns...we surely can help one another in many ways...but I don't believe that any of us ought to take on the responsibility of trying to warn everyone about every imaginable thing that is either a real, a potential or a presumed hazard. I agree with Mercedes here.
Kindest regards,
Zellie
> Geesh! you seem to have a negative response to everything. You respond and contradict others' 'good' or 'helpful' advice/intentions and manage to make everything so negative. This response and many you have posted are totally unacceptable, "killing of minds". Your opinion was not asked for. I know it's a 'free board' but for heaven's sake, don't scare people. We already have enough anxiety without having to hear our med's are "poisons".
>
> If a person makes a comment on what med has worked for them, please don't say things like "death" or "letal". Like I said, we have enough anxiety/depression and don't need to hear sh*t like that. Keep those to yourself. IMHO
>
> *************************************
>
> > the rediculous killing of minds when not appropriate, rather money-driven', that bothers me. if you may control the drug and use infrequently as intended---3 cheers. inderal? why do you think so many pop music icons have died from heroin? same deal. super-anxiety relief. right? or so they claim. put me to sleep for 26 hours--scripted to lessen lithium/imipramine 'tremor'. i'd still watch it and use only when a known need is overpowering.
> > it's like being a smoker---you'd best know cigs (a 'street-med as alcohol') or meds may be lethal and have 'cumulative' effects way down the line. if you close the deal, and infrequent inderal helps? great---start using it for every stressor, trouble you don't want to ever see, nor should you. IMHO.
>
>
Posted by maxx44 on January 2, 2004, at 22:50:16
In reply to Re: Max, stop being so negative! » maxx44, posted by Mercedes on January 2, 2004, at 21:28:06
let dr. bob decide my printable content---i feel your response inappropriate, or perhaps you just don't read throroughly---either the clearly stated risks on every shrink-med, or my posts'. i only deal with what i know, from myself and very numerous others. this is serious biz---you wish me flippant? not likely. not in your interest. savvy?
Posted by maxx44 on January 2, 2004, at 22:58:31
In reply to Re: Max, stop being so negative! » Mercedes, posted by Zellie on January 2, 2004, at 22:48:02
this is a med-board. i won't pat your back---i will tell you the med-negatives abounding on the net and experienced---in hopes you do not 'find yourself' gone. i've said 'if it works,it works', but i address those showing problems. i consider your response as 'flameing'.
Posted by maxx44 on January 2, 2004, at 23:21:25
In reply to Re: Max, stop being so negative! » maxx44, posted by Mercedes on January 2, 2004, at 21:28:06
as i said---my concern centers on 'do no harm'. meds can and do. as i concentrate on those with negative symptoms should i look like 'George Burns' and be a comedian on a med-board? i have a 26 year-old daughter on zyprexa for 2 years. she has diabetes---you make 'light' of this? i've expressed positives on many things. but the potential of crisis or life-long dependency matter to me more than your opinion---which does matter and is well taken. if nothing's hurting you, fine. if it is, i'm going to report from the net, observed experience of many others, and myself--it is no more negative than advising Grand Canyon campers to carry a flashlight, when walking the edge, at night. savvy?
Posted by Larry Hoover on January 3, 2004, at 10:49:26
In reply to re: atypical NMS, posted by maxx44 on January 2, 2004, at 18:18:18
> search 'neuroleptic malignant syndrome' (NMS), and 'atypical NMS'---when drs. speak of any neuroleptic they use a phrase, 'dopamine and/or dopamine serotonin' BLOCKADE---this is a misnomer as these drugs don't 'block' anything, rather Demolish the deep-brain production facilities and receptors of these key elements of 'self'. that's why those having used benzos or worse, neuroleptics, usually long-term but often even briefly, suffer the fate of always needing the drug. their born 'hardware' has been 'wiped'. scary? please, don't kill the messenger, as many would.
Well, I have no intention in killing the messenger, but I hope you won't mind if I challenge your declarations, and seek further information from you.
Quite contrary to what you declare above, neuroleptic malignant syndrome is generally associated with any drug which binds to the D2 dopamine receptor. There are exceptions, and those cases are considered to be idiosyncratic (due to factors present in the individual).
The total incidence of NMS is estimated to be 2 cases in 1000 (for all antipsychotic meds), and is generally accepted to be substantially less for the newer, so-called atypical antipsychotics, although data have not yet been sufficient for a numerical estimate.
NMS occurs 2/3 of the time within the first week of treatment, and almost without exception, within the first 30 days of treatment. Moreover, with appropriate medical care, the condition is considered to be fully reversible, upon discontinuation of the offending drug. There seems to be a trait susceptibility factor at work, so that those subjects having had one such occurence are substantially more likely to have another.
For more details, see:
http://www.nmsis.org/general_information.shtmlThe immediate occurrence of NMS (upon initiation of drug therapy) argues very much against your proposed "Demolish(ing of) the deep-brain production facilities and receptors of these key elements of 'self'", as does the immediate recovery therefrom. Moreover, neurotransmitters cannot, by any stretch of the language, be construed to be "key elements of 'self'".
Your experience with drugs in this class may well have been horrific, and I deeply sympathize with you. However, you cannot generalize from your experience to the population as a whole. In fact, despite more than forty years of observation and study of NMS, we still do not know what causes it, or why it strikes the individuals that it does.
I do appreciate that informed consent requires, obviously, that one become informed. However, disseminating hyperbole and exaggeration does not qualify. In the context of the experience of the population as a whole, NMS remains a rare occurrence. It is a risk of neuroleptic treatment (and a few other drugs, as well), and if patients read the information kit that should accompany any new prescription, they will be fully apprised of the symptoms of concern, as well as the need to seek emergency treatment should those symptoms occur. After one month has passed, one can reasonably stand down from that guarded stance.
Now, as to having the "hardware wiped".....
The hardware, receptors and neurotransmitters etc.???
I'm not even sure of what you speak of.
The only way that a permanent change can be effected is to have the DNA destroyed, or changed. All cells are constantly interacting with their environment. Everything outside an individual cell is environment to it.
Within a cell, everything is environment to the DNA.
The DNA actively modifies its environment, via mechanisms not yet known to us. Some genes will become more active, while others become less so, due to environmental clues. Unless the cell dies (Parkinson's disease is the death of very specialized dopamine-secreting cells in the substantia nigra, for example), it will respond to external clues in accordance with its own genetic complement.
If there is a sudden external change (drug initiation, or drug withdrawal, for example), there will be a lag time between the way the cell was set up to deal with the environment, until it can find a new comfortable way to deal with the environment. During that period of adaptation, there can be some (very) unpleasant experiences. In so many words, it takes time for the DNA to figure out what's going on external to it, and to adapt the cell to the new parameters.
Now, let's consider the use of benzodiazepines. Let's also assume they're used by someone with a reasonable argument for using them in the first place, e.g. anxiety interfering with their quality of life.
For many such people, long-term benzo use is the norm. But, over time, efficacy can diminish, or medical situations may develop, such that discontinuation of the med is required. (I'll ignore the presently commonplace benzophobia overcoming the medical establishment. That is an issue worthy of an essay, in and of itself.)
A person undergoing such withdrawal is very likely to have profound symptoms, characteristic of the opposite of the effects of the drug itself, so-called rebound phenomena. There may also be other unique effects of withdrawal.
Now, that person will not go back to being "normal" after withdrawal. They were, after all, experiencing quality of life (anxiety) issues in the first place. Moreover, it is entirely possible that their "disease" (I think the word is appropriate, as 'disease' arises from the Old French, diseasu, "not at peace"), can reasonably have progressed (the anxiety likely worsened over time, causing the individual to seek treatment initially, and aging has occurred during treatment), despite medical intervention, via benzos. There is ample reason to expect that such a person will be particularly uncomfortable after withdrawal of the benzo medication. To attribute such an experience to, how did you say it?, 'hardware' (having) been 'wiped', is without foundation, and smacks of fear-mongering.
Please do provide any information that you can about hardware wiping and demolished deep-brain production facilities, as I would very much like to become an informed consumer myself.
Regards,
Lar
Posted by maxx44 on January 3, 2004, at 16:55:24
In reply to re: atypical NMS » maxx44, posted by Larry Hoover on January 3, 2004, at 10:49:26
whew!---'the mark of gentlmen (person)is the ability to 'argue' points with no anger'---thank you for being in that catagory. i'll try and keep my rebuttal sequential to your points, and not assume your stated ignorance of NMS or ANMS as disengenuous.
1--you provide one link referring to the the D2 receptor, others refer to the D5. which is it?
2--the 'known' NMS reaction is 2%, not .2%, and this data comes from the drug cos., hardly a reputable source as the tens-of-millions suffering TD clearly show.
3--i was hit by ANMS, a 'spectral varient'. the keyword being 'spectral'. unlike classic NMS, which often resolves if treated promptly, unless you are among the 20% killed by it, or the even greater % left with 'rigidity (lead-pipe') and permanent altered mental status, ANMS may (in my case did) present at risperdal onset. but as it does not present as 'crisis', rather build with time, it's tricky for many shrinks to notice. i was given a trial for a dx of refractory depression.
4--given the 90 days of risperdal clearly resulted in lower motor-function, muscle-wasting, 'flattening', loss of some higher cognitive functions which persist 3 year's later
'scare-mongering' is IMHO an unjustified conclusion.
5--i repeatedly refer to the 'unique' aspects of each person. hardly overgeneralization.
4--both TD and 'protracted benzo withdrawal syndrome' are known, but not fully understood. but both indicate my point---if the dopamine hardware and receptors are not irreversibly 'wiped', or otherwise rendered inoperable, how is it that TD must be treated with L-dopa, bromocriptine, etc. for life?
5--your data is erudite. it comes, basically, from drug co. funded studies. answer me this. if you wished to partake of the imfamous sail-boat circumnavigation through the deadly 'lower 40's' latitude, would you hire a first mate who read a book or study, or a veteran of that journey?
6--'benzo-phobia' is not simply a 'fad'---rather ethical response, by Law, 'surgical procedure 'knock-out' or short term use are considered the normal use of same with rare exceptions. curiously, i am one, having suffered inoperable damage to my cardiac sphincter--precipitating 'life-threatening' panic. 'life-threatening panic?' my attacks terminate in severe convulsion or intense asthma, followed by being immobile for hours. it's the past indiscriminate scripting of benzos for less-needed use that has produced millions of 'accidental addicts'---these persons i address.
7--DNA? aside from its immune-system factors, to date it may only be shown to control the replication of protien molecules. it instructs a cell to be a liver cell vs. heart, etc.
8--tranqs and ADs are needed, sometimes, to mask symptoms of what now appears 'pathogen infestation' of nervous-systems. how else may you account for the dec. 1 newsweek data? 'when penicillin was introduced for syphilis, thousands of schizophrenics were Cured and released.?'
8--the role of cytoplasm, vs, DNA, is only recently being investigated. who knows?
9--erudition and experience of myself, children, relatives and well over 100 'group' participants obviously takes precedence over erudition alone.
i think that says it all------best wishes
Posted by maxx44 on January 3, 2004, at 18:22:42
In reply to re: atypical NMS » maxx44, posted by Larry Hoover on January 3, 2004, at 10:49:26
ps. i did neglect the key element of client age. young brains are more resilient to assault. but i must express some shock on your statement--'neurotransmitters are not considered part of 'self'. where on earth, or anywhere, did that come from? the entire medical approach to disorders centers on such. furthermore, you address NMS, not ANMS---it took 8 weeks before i realized i could not 'stoop'---my drs. considered my reportage, but at that time there was no body of evidence on ANMS---the immediate onset of incontinence and odd intermittent fever was ignored and 'rigidity' ascribed to the common
result of sleeping 16+ hours/day and weight-gain from risperdal, the only neuroleptic, save lico, long-discontinued, i've ever encountered. in vew of your 'errors of fact' (.2% vs. 2 % for NMS, neuroxmitters not being related to 'self'),i must consider your response either immature or disengenuous. either way, your elegant response is rendered as 'flawed' by content. as for 'scare-mongering'? i expect and deserve an apology. thank you, sir.
Posted by Larry Hoover on January 3, 2004, at 18:37:58
In reply to re: atypical NMS, posted by maxx44 on January 3, 2004, at 16:55:24
> whew!---'the mark of gentlmen (person)is the ability to 'argue' points with no anger'---thank you for being in that catagory. i'll try and keep my rebuttal sequential to your points, and not assume your stated ignorance of NMS or ANMS as disengenuous.
Where did I state I was ignorant about them? I was asking you for evidence.
> 1--you provide one link referring to the the D2 receptor, others refer to the D5. which is it?
I trust the linkage to D2 blockade. I have found no evidence for other dopamine receptor involvement, save one single study showing implicating D3 in combination with D2.
Mov Disord. 1996 Nov;11(6):726-8.
Imaging of dopamine receptors with [123I]iodobenzamide single-photon emission-computed tomography in neuroleptic malignant syndrome.
Jauss M, Krack P, Franz M, Klett R, Bauer R, Gallhofer B, Dorndorf W.
Department of Neurology, University of Giessen, F.R.G.
With the tracer [123I]iodobenzamide ([123I]-IBZM), it is possible to image dopamine receptor occupancy with single-photon emission-computed tomography (SPECT). We report follow-up examinations with IBZM-SPECT in neuroleptic malignant syndrome (NMS) to display D2-receptor availability in the acute phase and during the course of remission. A 27-year-old man was admitted with severe akinesia, rigor, tachycardia, fever, and elevated creatine phosphokinase level (CK) after neuroleptic medication. NMS was diagnosed, and treatment was started with dantrolene, amantadine, and dopamine agonists. IBZM-SPECT examination was performed on days 6, 34, 90, 107, 131, and 201. In the acute state of NMS, there was no binding of IBZM to D2-receptors. SPECT reached almost normal values on day 131, but clinical examination still showed a mild parkinsonian syndrome. With SPECT, the D2-receptor occupancy in NMS could be successfully shown in correlation with extrapyramidal signs. IBZM-SPECT may therefore serve to monitor D2-receptor occupancy in patients at risk for NMS.
> 2--the 'known' NMS reaction is 2%, not .2%, and this data comes from the drug cos., hardly a reputable source as the tens-of-millions suffering TD clearly show.
Are we talking about NMS or TD? They are very different entities.
I based my statistic on the following, which although the data are not presented in the abstract, the relevant stats are 27 cases of NMS out of 17,811 subjects. Caroff has probably published more articles about NMS than any other person, and is head of NMSIS.
Med Clin North Am. 1993 Jan;77(1):185-202.
Neuroleptic malignant syndrome.
Caroff SN, Mann SC.
Department of Psychiatry, University of Pennsylvania, Philadelphia.
Neuroleptic malignant syndrome is a rare but potentially fatal reaction associated with neuroleptic drugs. It occurs in about 0.2% of patients treated with neuroleptics. Risk factors include previous episodes, dehydration, agitation, and the rate and route of neuroleptic administration. Although NMS has been reported in patients with diverse psychiatric diagnoses, as well as in normal subjects, patients with organic brain disorders or mood disorders, particularly when receiving lithium, may be at increased risk. Standardized criteria for the diagnosis of NMS have been developed and emphasize the classic findings of hyperthermia, muscle rigidity, mental status changes, and autonomic dysfunction. The syndrome lasts 7 to 10 days in uncomplicated cases receiving oral neuroleptics. Treatment consists primarily of early recognition, discontinuation of triggering drugs, management of fluid balance, temperature reduction, and monitoring for complications. Use of dopamine agonists or dantrolene or both should be considered and may be indicated in more severe, prolonged, or refractory cases. Electroconvulsive therapy has been used successfully in some cases and is particularly useful in the post-NMS patient. As a result of these measures, mortality from NMS has declined in recent years although fatalities still occur. Neuroleptics may be safely reintroduced in the management of the majority of patients recovered from an NMS episode, although a significant risk of recurrence does exist, dependent in part on time elapsed since recovery and dose or potency of neuroleptics used. Data drawn from clinical observations and basic studies support the primary role of an acute reduction in brain dopamine activity in the development of NMS. Additional studies of facilitating cofactors may lead to innovative risk-reduction strategies and the development of safer neuroleptic drugs.
That isn't drug company data.
How about this study, where the incidence was 0.02% out of nearly 79,000 subjects?
Eur Psychiatry. 2000 Aug;15(5):330-3.
Frequency of neuroleptic malignant syndrome in a large psychiatric hospital in Moscow.Spivak B, Maline DI, Kozyrev VN, Mester R, Neduva SA, Ravilov RS, Weizman A.
Research Unit, Ness Ziona Mental Health Center, POB 1, Ness Ziona 74100, Israel.
A ten-year prospective survey of neuroleptic malignant syndrome (NMS) was performed in a major psychiatric hospital (1,510 beds) in Moscow. All inpatients who developed a persistent and severe extrapyramidal rigidity accompanied by fever after exposure to neuroleptic medication were screened for NMS. The diagnosis of NMS was established according to Levenson's criteria and at a later stage all NMS cases were reevaluated using the DSM-IV research criteria. Data on age, gender and psychiatric diagnoses were analyzed. Of the 78,708 inpatients treated with neuroleptic agents, 19 separate patients had an episode of NMS, for a frequency of 0.02%. Mortality rate was 10.5% (2/19 patients). Of the three potential risk factors studied, only young age (</= 25 years) was significantly associated with an increased frequency of NMS (P < 0. 01). The low rate of NMS found here compared to studies in other countries may be due to the stringent demands for NMS diagnosis. More large-scale prospective studies including detailed clinical and laboratory data are needed to clarify these differences and their impact on the prevalence and risk factors of NMS.
> 3--i was hit by ANMS, a 'spectral varient'. the keyword being 'spectral'. unlike classic NMS, which often resolves if treated promptly, unless you are among the 20% killed by it,
Untreated, fatalities might approach that number.
> or the even greater % left with 'rigidity (lead-pipe') and permanent altered mental status, ANMS may (in my case did) present at risperdal onset.
If it does not present at onset of treatment, it is virtually certain to not be NMS.
> but as it does not present as 'crisis', rather build with time, it's tricky for many shrinks to notice. i was given a trial for a dx of refractory depression.
I am sorry your drug trial was such a trial for you. I would suggest that the more general term EPS might apply to your situation. I am not trivializing your experience.
> 4--given the 90 days of risperdal clearly resulted in lower motor-function, muscle-wasting, 'flattening', loss of some higher cognitive functions which persist 3 year's later
> 'scare-mongering' is IMHO an unjustified conclusion.The existence of individual adverse effects is not generalizable....that is all I ever said. Moreover, the absence of temperature disregulation argues against a diagnosis of NMS.
> 5--i repeatedly refer to the 'unique' aspects of each person. hardly overgeneralization.
No argument there. However, incidence remains a point of contention. I am not a drug company shill. Serzone nearly killed me. However, I recognize the incidence of liver toxicity is low, and I accept that adequate warnings are in place.
> 4--both TD and 'protracted benzo withdrawal syndrome' are known, but not fully understood.
Are we talking about TD now?
> but both indicate my point---if the dopamine hardware and receptors are not irreversibly 'wiped', or otherwise rendered inoperable, how is it that TD must be treated with L-dopa, bromocriptine, etc. for life?
Long-term neurotoxicity is quite another subject. And it is far more complex a phenomenon than is your "wiped".
> 5--your data is erudite. it comes, basically, from drug co. funded studies. answer me this. if you wished to partake of the imfamous sail-boat circumnavigation through the deadly 'lower 40's' latitude, would you hire a first mate who read a book or study, or a veteran of that journey?
Damned by faint praise. I doubt the Moscow data was drug company funded.
> 6--'benzo-phobia' is not simply a 'fad'---rather ethical response, by Law, 'surgical procedure 'knock-out' or short term use are considered the normal use of same with rare exceptions. curiously, i am one, having suffered inoperable damage to my cardiac sphincter--precipitating 'life-threatening' panic. 'life-threatening panic?' my attacks terminate in severe convulsion or intense asthma, followed by being immobile for hours. it's the past indiscriminate scripting of benzos for less-needed use that has produced millions of 'accidental addicts'---these persons i address.
Addiction is quite another matter. I am quite convinced of the potency of benzo withdrawal. I frequently refer people to http://www.benzo.org.uk
> 7--DNA? aside from its immune-system factors,
???
> to date it may only be shown to control the replication of protien molecules.
That is all DNA codes for, proteins. Replication is, strictly speaking, a function of RNA. However, to totally block transcription of DNA, or to cause it to fail entirely (that's really the only mechanism for the destruction you imply), irreversible chemical changes in the DNA must occur.
> it instructs a cell to be a liver cell vs. heart, etc.
Differential expression of DNA determines cell type. I was speaking to feedback regulation of gene expression.
> 8--tranqs and ADs are needed, sometimes, to mask symptoms of what now appears 'pathogen infestation' of nervous-systems. how else may you account for the dec. 1 newsweek data? 'when penicillin was introduced for syphilis, thousands of schizophrenics were Cured and released.?'
I fail to see the relevance of syphilis or penicillin to the discussion at hand, atypical neuroleptic malignant syndrome. In any case, we need not necessarily know the etiology of a symptom to determine an efficacious intervention or treatment. A witch doctor invoking the spirit of an herb in the laying of a spell to treat illness may well be administering a plant-based drug. Does it matter which is correct, if the patient recovers?
> 8--the role of cytoplasm, vs, DNA, is only recently being investigated. who knows?
The cytoplasm is the only environment the DNA will ever have, so long as the cell lives.
> 9--erudition and experience of myself, children, relatives and well over 100 'group' participants obviously takes precedence over erudition alone.
Again, we come to incidence. Self-selection bias could not play a part in your group?
> i think that says it all------best wishes
I still am looking for data or arguments to support your previous declarations.
Regards,
Lar
Posted by maxx44 on January 3, 2004, at 19:36:51
In reply to re: atypical NMS, posted by Larry Hoover on January 3, 2004, at 18:37:58
see xxx or the 1st google page on NMS---rate of NMS =.2-2.2%--u of p is just one bit. there are many. i learned a lot from your post---re: muscle/bone damage, which searching led to atypicals and 'slow NMS'--exactly what got me. yet you have said 'zip' on ANMS. and if 'trials or stats' reveal up to 2.2% mortality in some NMS stats, i feel it reasonable that the actual number is higher. why did you quote the lowest figure possible? i've seen one reference to a teen with risperdal induced NMS and the accompyning statement indicateing a 7% rate of onset for teens. who would script risperdal for what ritalin was 'safely-used-for'? now known as lethal in significant numbers? a dr. the tech aspects of your response deserve a separate post. later--'playoffs, you know. the bucs may be dead, this year, so now i root for the panthers. best wishes
Posted by Larry Hoover on January 3, 2004, at 19:56:56
In reply to re: atypical NMS, posted by maxx44 on January 3, 2004, at 18:22:42
>furthermore, you address NMS, not ANMS---
There is not one single reference to atypical neuroleptic malignant syndrome on Pubmed/Medline. Forgive me for failing to find evidence for something that has not been published under peer review criteria.
I stand by my incidence statistics for NMS.
I am sorry you went through what you did.
Lar
Posted by maxx44 on January 3, 2004, at 20:11:53
In reply to re: atypical NMS » maxx44, posted by Larry Hoover on January 3, 2004, at 19:56:56
appeciation accepted---now keep searching---you have hardly exhausted your resources--you want truth or patronization?
Posted by Larry Hoover on January 3, 2004, at 20:35:28
In reply to re: atypical NMS, posted by maxx44 on January 3, 2004, at 19:36:51
why did you quote the lowest figure possible?
I didn't. I quoted one midspectrum, with a large N size. I tend to ignore outlier stats, or those based on small samples. I am a professional scientist, and I am using my scientific judgment. I originally quoted a median value.
I supplied a reference with a larger N, and a lower incidence, of 0.02%. (19 cases out of 78,708), but that is lower than the more typical figure.
Each reference with higher incidence had much much smaller N, some as few as 7 subjects.
Lar
Here's another with large sample, small incidence.
Can J Clin Pharmacol. 2003 Fall;10(3):111-3.
Neuroleptic malignant syndrome in Mexico.
Montoya A, Ocampo M, Torres-Ruiz A.
Brain Imaging Group, Douglas Hospital Research Centre, McGill University, 6875 Boulevard LaSalle, Verdun, Quebec H4H 1R3, Canada. [email protected]
BACKGROUND: Neuroleptic Malignant Syndrome (NMS) is an uncommon but potentially fatal complication of antipsychotic and neuroleptic drug treatment. OBJECTIVES: This study estimated the frequency, clinical presentation, and outcome of NMS in a referral center for neurological, neurosurgical and psychiatric disorders in Mexico. METHODS: The authors conducted a thorough search of psychiatry, neurology, neurosurgery and intensive care unit records for cases of NMS during the 10-year period between 1990 and 1999. They examined the clinical features, course and treatment of the NMS episodes, and performed a follow-up survey for residual symptoms and clinical outcome. The mean time to follow-up assessment was 36 months. RESULTS: A total of eight of 4831 neuroleptic-treated patients had an episode of NMS (incidence 0.165%). Seven of the eight patients were treated with haloperidol. Other neuroleptics agents associated with NMS were depot pipotiazine palmitate and levomepromazine maleate. One patient received lithium concomitantly. No fatal outcome was found. Only one patient developed persistent clinical sequelae, consisting of extrapyramidal and cerebellar symptoms, three years after the NMS episode. CONCLUSIONS: The slightly low frequency of NMS found in this study compared with studies conducted in other countries may be attributable to the advent and use of newer atypical antipsychotics in Mexico, the rigorous demands for NMS diagnostic criteria and the lack of familiarity with the diagnosis between physicians.
Posted by maxx44 on January 3, 2004, at 20:49:28
In reply to re: atypical NMS » maxx44, posted by Larry Hoover on January 3, 2004, at 19:56:56
2 sources/ vs. hundewds and years tracking them? i have said i am no dr. if you have credentials, please state them. there are tons of ANMS articles and studies for all to see---just hear me out, mate---i've done 4 years of net research. ususally an abstract will do. sometimes you have to learn the jargon and history of a study. i don't know what to say to a post proclaiming validity from 2 web-sites. seems rather superfluous to the obvious conclusions of anyone knowing there are hundreds of related sites to quote. and learn from.
Posted by Larry Hoover on January 3, 2004, at 21:07:36
In reply to re: atypical NMS, posted by maxx44 on January 3, 2004, at 20:49:28
> i've done 4 years of net research.
I asked you for references, links....
> i don't know what to say to a post proclaiming validity from 2 web-sites.
????
> seems rather superfluous to the obvious conclusions of anyone knowing there are hundreds of related sites to quote. and learn from.
Then show me.
Posted by maxx44 on January 3, 2004, at 21:12:01
In reply to re: atypical NMS » maxx44, posted by Larry Hoover on January 3, 2004, at 20:35:28
i see your approach, your 'scientific' style. you are not 'involved' with these drugs personally---rather, looking at them. your flow of data is erudite---like a marine reading of combat vs. being there. and usually funded by the very cos. promoting the drug. i may bee a loof, but i an longer an academic fool.
Posted by Larry Hoover on January 3, 2004, at 21:42:31
In reply to re: atypical NMS, posted by maxx44 on January 3, 2004, at 21:12:01
> i may bee a loof, but i an longer an academic fool.
???
Posted by zinya on January 3, 2004, at 21:53:18
In reply to Re: effexor changes in brain funxn. Help?, posted by mom_cheeks on December 27, 2003, at 8:53:00
greetings after a few weeks' absence here, and happy new year to all (Kim D in particular - how goes it?),
As some hear will know but newcomers won't, i started Effexor last May 30 and probably hold the record to date for slowest titrations upward (splitting capsules to move up at slower increments than the "norm"), arriving at 150 mg by late July and staying there til Labor Day - 6 weeks at 150, and then 2 unrelenting SEs obliged me to realize they simply weren't going away - as they'd lasted 3 months and the 2nd of the two became alarming.
I just read two of your posts, already mc - and also gummybear's uptake (that's different from reinhibitor uptake :)) -- sorry, bad joke, lame head here, fairly flued out here in recent days ...
Anyway, i read your posts and i confess to having felt some envy. I had the same sense of 'crossroads' you did upon first embarking on Effexor, hoping against hope after numerous other failed AD attempts over 15 yrs off and on, and I am truly happy for you that it turned out to be exactly the best scenario. It's so important that such stories be told too. I've been monitoring this site off and on for over a year (at first it made me delay starting the Effexor for months in apprehension at teh SE's but then i came to a sense of hitting further 'bottom' and started also with a "what the hell" kind of "nothing ventured" added sense at the beginning.
But the two biggies for me in SEs include one that's relevant to your post here, so i write to suggest a modification to a statement of yours to mMarie...
Namely, regarding the sweats. For me they started at 37.5, which was my 2nd level (I started with half a min. dose - 19 mg - half the granules of a capsule) ... They started to taper off after a couple of weeks at 37.5 (staying at least 2 weeks at each new level) and then going up next to 56 first before on to 75, but from 75 mg onward, the sweating was daily and relentless. Night sweats to the point of waking me at 3 am having to change clothes cuz nightshirt, undies, sheets, pillow . everything just sopping... By day, i couldn't even dress to go somewhere at times because i'd put on clothes and sweat inside them so much i couldn't stand it and would have to just rip (well...) my clothes off and call to cancel the whatever and return to wearing virtually nothing. I couldn't even dust a shelf without an instant sweat that would start dropping sweat on the furniture and making the enterprise counterproductive, and so i'd quit. That level of sweating lasted from some point in June until Labor Day and beyond.
At Labor Day (roughly) a second phenom added alarm to the overwhelming annoyance of the sweating. At 150 mg level in particular i started having heart rate/palpitations i'd never had (always low b.p.) to the point that just weekly gardening for an hour - i mean GARDENING for heaven's sake, a leisurely albeit exertion-using activity, was impacting me as if i'd just run the marathon. I not only would be dripping with sweat (at 5 pm, with ocean breezes etc) within 5 minutes but after working for an hour-plus, my heart would be racing so much i sometimes had to rest 15 min. befor continuing but i always ended up with such a scarily-exhausted palpitating heart that i had to start using a stool under the shower to sit on to then wash my hair for fair i would collapse, so heart-racing exhausted from the gardening. I began to realize i couldn't risk REAL aerobic exercise cuz the Effexor was turning non-aerobic into aerobic already... After a month-plus of that not letting up, that was, alas, I felt, a signal i could no longer think would go away.
The third thing was that i had yet to feel any boost to my energy, the very thing that had made my md. choose Effexor instead of other ADs so as to get the norep. effects for energy. Never felt a sustained energy though i did manage to rally for those weekly gardenings and -- some weeks -- able to walk daily on the non-gardening days, but then would have relapses energy-wise.
What makes me write here is hearing a global generalization. While i agree with those who have said here in recent posts, it's not productive to hear generalizations made to scare users, i also think it's ill-advised to make global assurances.
If there's one thing this board has taught me, it is just how truly unique each of our body chemistries are. There is literally no way of predicting whether one person is going to get over their sweats or not, lose sleep or not, gain weight or not, feel the postiive effects of E (or anything else) or not, etc etc. It's all gross generalizing that can set up expectations for that which winds up sabotaging -- either by discouraging some from trying or others from listening to their bodies when maybe they need to.
I don't know. I sure would have liked Effexor to work for me. It helps that i kept a journal of effects all the while so as to keep me from 'grass-is-greening' now as i think "gosh, maybe i could have stuck it out further and gotten to some "oasis" hurdle point. But i could also have prolonged the bad SEs dangerously. Who knows. Ultimately, it's judgment calls. And i think one thing each person needs to develop is real 'knowledge' of their own body, its signals, its antenna, its limits and capacities...
Because no one else can tell you whether *your* SEs will end or not, whether it would eventually start giving you rewards or not.
It's stunning really to realize just how unique each experience is although specific isolated SEs are shared ... but then not others, such that no one person has the same SET of pros and cons on these truly paradigm-shifting drugs for the brain...
I started tapering off at Labor Day, going down SOOO slowly that i'm still now not 100% off. I'm down to taking -- ready for this? -- 6 mg every 3-4 days. :)) ALMOST nothing, but not nothing. Cuz absolute nothing isn't quite ready yet. I start to feel a bit of brain zaps on day 3 or 4 since last dose, and realize i should take another... But a few weeks ago, that same was true of 9 mg and before that it was 9 mg every night still, 12 mg before that, 18mg ...
What this site had taught me was that going off was/is even trickier than going on, so i've taken my SLLLOOOOW-going entry and made an exponentially slower-going exit... For the most part, it's spared me the worst kind of brain zaps others had by exiting faster. I of course didn't miss all the brain zaps, but the never were "scary" at least.
And the thing that was scary - the racing heart after gardening - started leaving again by the time i got down to about 50 mg again... The sweating lingered on -- reduced but still annoying - to at least after 37.5 (not checking my journal here, from memory) ... I still occasionally getting a sweating thing that was unprecedented for me prior to Effexor, but nada compared to what those months on the Effexor onramp had been like.
2% of users, the bulletin says, quit Effexor in controlled studies due to sweating. So there's others out there having my response.
It happens, just like shit happens.
I hope this comes across mostly as supportive - as my intent is only to encourage everyone not to overgeneralize based on their own experience while being supportive for each other and helping each other recognize certain SEs as being, indeed SEs... rather than something else...
The whole sweat thing leads me to a quandry still though about the functioning of these drugs which is in reaction to the post of mMarie's which you are responding to. I'll post a separate reply to it in order to pose my confusion about something she said ...
wishing you all well and good '04s...
zinya
Posted by Larry Hoover on January 3, 2004, at 22:01:01
In reply to re: atypical NMS, posted by maxx44 on January 3, 2004, at 20:49:28
> there are hundreds of related sites to quote. and learn from.
How about supplying your favourites? From among the hundreds?
Lar
Posted by maxx44 on January 3, 2004, at 22:15:24
In reply to re: huh what? » maxx44, posted by Larry Hoover on January 3, 2004, at 21:42:31
typing and nfl playoffs don't mix, sometimes. i may be a loof, (anolog) but no longer an academic fool. living it surpasses reading of it. as for researchers? well they get special consideration. now---if you are this research scientist and your goal is helping the millions with infested nervous-systems---great. if not, why not shift your specialty to pathogen detection and whacking? we need real help, sir, asap. and you need ours as well. the fact you've 'quantified' your view, experimentaly, is commendable. i'm better an astro-physicist vs. this board. still, you're 'fudgeing'. 2 google references from many? there's so much more than that---from in-depth specialists works to nami---
Posted by zinya on January 3, 2004, at 22:26:05
In reply to effexor changes in brain funxn. Help?, posted by mMarie on December 26, 2003, at 14:45:24
hi Marie!
i've just given a long-winded re-intro of myself above... and where i prefaced how i was going to write you here with a question about this statement of yours:
>Hot flashes are directly linked to norepinephrine. Blocking NoreP will prevent the hot flash. Effexor has been successful in treating menopausal women b/c it is a >NoreP Reuptake Inhibitor. Like Serotonin, more NoreP floats around in the brain as it has been blocked from re-uptake. Atleast this is how I understand it.
My own entry into Effexor led me to try to understand the Norep. component most of all since it was <i>the</i> reason my md chose Effexor and the lure was that it would be an energy aide since my biggest single problem was ZERO energy. But this particular account confuses me, unless (and probably) it's just yet another sign of how much this same drug can have reverse effects on separate individuals.
For me, sweating occurred and remained (as i just described in some detail on previous post) while ON Effexor, and tapered off since quitting. So it's hard to see that as fitting with the above description of effects.
But, even without my own alternate experience, it's not clear to me (but this could all be the still flu-addled brain i'm trying to emerge from today) how the theory you described works. If BLOCKING Norep prevents hot flashes (and sweating, presumably), then that means Norep promotes it. So taking a "reuptake inhibitor" for Norep should mean (shouldn't it?) that more of it "floats around in the brain," wouldn't that precisely coincide with my experience of Norep promoting sweating ... And so WHY would it be prescribed for menopause???
Unless, again, it perversely has opposite effects for different individuals or different situations where maybe menopause is itself some unique biochemical circumstance which reverses cause-effect relations???
Well, i feel like i'm just babbling here, and understanding the theory of this probably interests only a few, but if anyone has any light to shed on this, i'd appreciate it.
>Question: Could the Effexor after 3 months of only 37.5mg have permanently altered my brain function? Could I be producing more NoreP--Could I be out of balance? >How long does it take the chemical substances in the brain to return to the state they were in PRE-Effexor OR CAN EFFEXOR CAUSE PERMANENT CHANGES?My own response to your query here, Marie, would be similar to what i just wrote in the post above (to moms_cheeks, i think it was - or Zellie, who both seemed to have similar experiences to date, if i recall right) ... Namely, yes and no :)) -- it might or it might not. That would be my best guess. :)
Sorry to suggest such an unhelpful response but i don't think anyone who's being honest (which most doctors alas, are not, and the drug co's certainly are not) they really don't know what the risks for a given individual are nor the potentials cuz we're in an area of brain chemistry here that is so profound and basic to the whole body functioning, so intersected with everything, that it's unknowable.
I'm essentially "off" Effexor again and i don't THINK i've had any 'permanent' personality or other changes from my six months total on it ... What i still deal with is zero -- or rare intermittent -- energy, which there was no sign the Effexor was really changing, but on balance i THINK it's right for me to be off of it, though god i wished it could have done for me what it seems to have for mom's cheeks and Zellie (if i'm remembering the right names, both of you being new to me, i think)...
well, that's it for now -- also stll dealing with carpal tunnel which seems to be an SE from Effexor as well and/or from Effexor withdrawal perhaps - it started back in October while i was on the downcycle at around 75 mg. It IS known to be associated in at least some studies with menopause suggesting it is estrogen-related, and the only previous time i had carpal tunnel i too had had an upheaval in my estrogen levels. I'm deducing from this reoccurrence that Effexor impacts our hormones' functioning too (how couldn't it?) and so the return of carpal tunnel after 3 yrs must not be a coincidence....
I've been quite vulnerable immune-system-wise lately, it seems - this latest flu hitting me hard being the latest example but it's been a whole year like that it seems... But who knows what's cause and what's effect?
good questing and living to you all,
zinya
Posted by maxx44 on January 3, 2004, at 22:30:40
In reply to Re: effexor changes in brain funxn. Help? » mom_cheeks, posted by zinya on January 3, 2004, at 21:53:18
generalizations designed to scare? then what is this tale of idiosycratic sweat, save the same? just honest reportage which may help. yes, it's negative---what sense in responding to happy solutions? no problem? no interest.
Go forward in thread:
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
[email protected]
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.