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Medical Forum / General / General / February 2005

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Mode of action of Clonazepam

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homer321@gmx.net - 23 Feb 2005 12:49 GMT
Hello everyone,

Dr. Cheney, one of the world's most reknown researchers and physicians
for Chronic Fatigue Syndrome (CFS), recommends his patients to take
Clonazepam.

See e.g. here: http://www.cfsresearch.org/cfs/cheney/33nf.htm .

He thinks that it protects the patients' brains against what he calls
"excitatory neurotoxicity".

I would be very grateful if one or some of you could take the time to
have a look the above-named page and provide an expert's view.

The reason for my interest: As a patient with CFS, I've been taking
Clonazepam for several years because of this recommendation, and
because I think that it improves my quality of sleep. However, I'm not
sure about the sleep effect (I'd have to withdraw from the medication
and try it again to verify the effect). And I have a bit of an
unpleasant feeling taking Clonazepam because every doctor I go to is
quite aghast that I'm taking it!

How strong do you think are the scientific grounds for Cheney's
opinion? Does it seem plausibel to you?

Thanks in advance for all comments!

Kind regards

Holger
ironjustice@aol.com - 23 Feb 2005 17:47 GMT
Long and winded explanation for a problem with iron levels in the brain
..

The drug in question is an iron binder ..

It works by disallowing the oxidation of the iron ...

Epilepsy Res 2001 Jan;43(1):59-66

Effects of antiepileptic drugs on rat platelet aggregation: ex vivo and
in vitro study.

Rajtar G, Zolkowska D, Czechowska G, Kleinrok Z
Department of Pharmacology and Toxicology, Medical University,
Jaczewskiego 8, PL 20-090, Lublin, Poland.

The influence of conventional antiepileptic drugs (valproate,
phenobarbital, diazepam, clonazepam, carbamazepine and
diphenylhydantoin) on rat platelet activation induced by arachidonic
acid (AA) or adenosine-5'-diphosphate (ADP) was investigated both ex
vivo and in vitro on platelet-rich plasma (PRP). It was found that only
diazepam, and to a smaller extent clonazepam, impaired rat platelet
function. These benzodiazepines did not affect ex vivo platelet
aggregation induced by ADP but dose-dependent inhibition of platelet
aggregation and malondialdehyde (MDA) synthesis were observed, when the
platelets were stimulated with AA (ED(50) of diazepam for aggregation
was 2.7 mg/kg and that for MDA synthesis - 3.9 mg/kg). In in vitro
study, diazepam was found to be a potent inhibitor of AA-induced
platelet aggregation (IC(50) 1.2 microg/ml) and MDA synthesis (IC(50)
4.0 microg/ml). Higher concentrations of diazepam were required to
inhibit ADP-induced aggregation (IC(50) 29.0 microg/ml). Clonazepam
also exhibited a concentration-dependent inhibitory effect on
AA-induced platelet aggregation and MDA synthesis but this effect was
weaker when compared to diazepam. The present data demonstrate that
diazepam possesed a strong inhibitory effect on rat platelet
activation. The correlation between the reduction of platelet
aggregation and the synthesis of MDA may suggest that the observed
effect of diazepam is due to the inhibition of the cyclooxygenase
pathway of the AA metabolism in platelet.

PMID: 11137387, UI: 20578853

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