Posted by Sunnely on December 4, 2000, at 19:46:08
In reply to Re: Olanzapine and side effects » Sunnely, posted by SLS on December 4, 2000, at 6:45:28
> Is there a cross-sensitivity to NMS? To what degree?
>
>
> - Scott+++++++++++++++++++
Hi Scott,
Although the exact mechanism of NMS remains unclear, it does not appear to involve a hypersensitivity reaction. There have been reports of patients who developed NMS from one phenothiazine antipsychotic and were successfully re-challenged with another phenothiazine antipsychotic. Also, there have been reports of patients who developed NMS from one medication and were re-challenged successfully, although with extreme caution, with the very same antipsychotic drug that caused it.
It has been postulated that NMS is due to the central (nervous system) dopaminergic blockade leading to an an acute state of dopamine deficiency. Therefore, any drug with the ability to block dopamine receptors such as the antipsychotics, is also capable of causing NMS. So, every time one is prescribed an antipsychotic drug, there is always the risk for NMS, but of course, this does not always occur. A number of contributing factors play some role in its development. Another possible scenario for NMS to occur is when an antiparkinsonian drug is abruptly discontinued. So, patients with Parkinson's disease and on antiparkinson drug, may be at risk for NMS if the antiparkinson is abruptly discontinued. This action leads to a state of acute dopamine deficiency.
Other drugs (not antipsychotics) have also been reported to cause NMS such as lithium, anti-emetics (Compazine, Torecan, Tigan, Reglan), antidepressants (tricyclic antidepressants, MAOIs, and yes, SSRIs).
The risk of NMS on someone taking an antipsychotic drug becomes higher if certain factors are also involved. These factors include but not limited to: 1) starting the antipsychotic drug at high dose; 2) rapidly increasing the dose; 3) dehydration; 4) agitation; 5) affective disorders (bipolar disorder, depression) higher than schizophrenia; 6) presence of organic brain syndromes (e.g., dementia, history of brain injury); 7) concurrent use of lithium. Younger males seem to be affected more than females. There is no consistent evidence that one antipsychotic drug or class is more or less likely to produce NMS.
NMS usually does not occur overnight. It was suggested that about 70% of NMS cases follow a spectrum of events. Usually, the premonitory signs are confusion, mutism, and catatonia. There may be accompanying muscle rigidity or tremor (EPS). So, if someone on antipsychotic drug develops these symptoms, especially the combination of mutism or catatonia and EPS, THINK NMS and stop the antipsychotic immediately. If the antipsychotic drug is stopped immediately and with suppportive care, you can almost always prevent the NMS from developing into a full-blown stage, when it becomes more serious and increased risk of fatality.
The 4 cardinal clinical features of a full-blown NMS are: 1) Hyperthermia (markedly elevated body temperature, 104 F or higher); 2) Muscular rigidity (e.g., "lead-pipe" rigidity; patient can't move, can't talk, can't swallow); 3) Autonomic instability (e.g., blood pressure fluctuating, rapid pulse, rapid respiration, profuse sweating, incontinence); and 4) Altered consciousness (e.g., confusion, agitation, mute, frightened facial expression, lethargic, stuporous, delirious). Although not diagnostic of NMS, in one study, 92% of patients who developed NMS had elevated levels of CPK (creatine phosphokinase). CPK is a muscle enzyme and a sensitive marker of muscle injury (e.g. marked muscular rigidity). Death from NMS is usually due to acute kidney failure or aspiration pneumonia.
poster:Sunnely
thread:938
URL: http://www.dr-bob.org/babble/20001130/msgs/49922.html