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re: atypical NMS

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

 

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poster:Larry Hoover thread:13781
URL: http://www.dr-bob.org/babble/20031231/msgs/296113.html