I want only honest and INSTINCTIVE and TRUTHFUL replies without the respondents resorting to Google searches and/or PubMed or other several sources of information available on the Internet at the click of the mouse. I want Neurologists at all levels of medicare, primary or secondary or tertiary to give a clear answer with the dose(s) they employ and the duration of their recommendation of atenolol, used either singly or in combination with other migraine preventing drugs.
I want to remind all readers that the role of atenolol is the best guarded secret of migraine prophylaxis!!!
I also want PHYSICIANS/NEUROLOGISTS/PHARMACISTS/PHARMACOLOGISTS who believe that atenolol is only an anti-hypertensive agent to clearly declare their conviction.
Please do not answer if you, for some reason, cannot be a professionally honest SCIENTIST / PRACTITIONER.
Atenolol can be useful, anyway there are not controlled trials about its use in Migraine. If you consider that the vast majority of migraine sufferers are young women a drug wich decrease the blood pressure and bradicardia is not the best option.
See my paper about Topiramate but, by the way, does`t produce weight gain.
Sergio, I am not going to do the hard work for you...
Explore about Atenolol yourself...
your assumptions are incorrect...
I use frequently atenolol for migraine, from 25 mg to 50 mg bid.
Atenolol is one of the B-blockers with long half-life....
I have no idea about how atenolol works in migraine. I suppose a central or microvascular action that blocks or inhibits activation of neurogenic inflammation
I am afraid, your supposition is incorrect.
Atenolol has no known central CNS/Brain neuronal modulation function. Its only side-effect is insomnia, which is indeed a central CNS/Brain related phenomenon.
Pushing forth, we really do not know how propranolol also works to prevent migraine attacks.
Contrary to what most migraine researchers say, there is only one mechanism of action for all drugs that prevent migraine. We are at A and that mechanism will become apparent when we reach Z.
If you read my book as below, you could reach Z point much earlier. As you are young, you will benefit from what I call the investment of a lifetime for a Neurologist -- that is buying and reading my book again and again right from the fist page.
Today, I have posted a complete article on my home page regarding cortical spreading depression. I think you should read that first.
The efficacy of atenolol in preventing migraine, IS THE BEST KEPT SECRET OF MIGRAINE THERAPEUTICS AND MIGRAINE PATHOPHYSIOLOGY.
You can understand migraine only when you understand the adaptive function of vasopressin -- new question to be put up today. Prof. Welch (Cephalalgia), in 1994, requested me to write about vasopressin more than 20 years ago,
It most likely acts on the peripheral components of the trigeminovascular reflex which is one of the three proposed mechanisms of migraine headache. (pointing towards migraine as heterogeneous disorder.) As does Metoprolol, which is not penetrating into the CNS as well. Given there are valid studies, I prefer to use Metoprolol. (in my experience, patients on Atenolol have no further benefit.)
Dirk Ulbricht · 37.15 · Centre Hospitalier Emile Mayrisch
Dear Dirk:
Your comment on the utiltity of Atenolol for preventing migraine attacks is completely incorrect.
Metoprolol does not penetrate into CNS -- you are completely wrong.
How is the peripheral component of the trigeminovascular system being activated?
How is metoprolol preventing peirpheral activation of the trigeminovascular system?
The concentration in the CSF of the three lipophilic beta-adrenoceptor blockers, propranolol, oxprenolol and metoprolol, approximated to the free drug concentration in the plasma, and was a poor predictor of brain concentration. These three lipophilic beta-adrenoceptor blockers appeared in brain tissue at concentrations 10-20 times greater than that of hydrophilic atenolol. The approximate brain/plasma ratio for propranolol was 26, for oxprenolol 50, for metoprolol 12 and for atenolol 0.2. Br J Clin Pharmacol. 1981 Jun; 11(6): 549–553.
Please do not reply without references to support your own view-point.
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