heya guys! just a quick brain spin here, that made me wonder, please, if i get this the wrong way, id love to be corrected.

the pain in our CH attacks, comes from the dilation of certain blood vessals, hitting the nerves on the side of our heads (either left, right or both) , and branching out to the eye, jaw, neck and nose. how the pain gets there is something else, i won't get into that.

the way imigran/imitrex works, is because it constricts those dilated nerves, so they dont push against the nerves anymore, and making the pain go away.

from what this looks like, our main focus point is to keep those blood vessals from dilating in the first place, if we can keep them from dilating and hitting the nervous system, then that would certainly make peoples lives much easier.

here is where i get confused.

the way verapamil and beta blockers work, is that they DILATE blood vessals, wich in turns lowers blood pressure etc etc. 

so why do we take verapamil and beta blockers?
and why are they working for so many people?

voluntarily dilating the blood vessals doesnt sound like a great idea if you are suffering from CH.

im sure im missing something, that would explain this confusing fact. maybe by manually dilating of blood vessals trough medication makes the dilation the CH gives, bearable?

matt

There are different classes of calcium channel blockers, and they work on BP in different ways. Verapamil is of this class:


Quote:

Phenylalkylamine calcium channel blockers are relatively selective for myocardium, reduce myocardial oxygen demand and reverse coronary vasospasm, and are often used to treat angina. They have minimal vasodilatory effects compared with dihydropyridines and therefore cause less reflex tachycardia, making it appealing for treatment of angina, where tachycardia can be the most significant contributor to the heart's need for oxygen. Therefore, as vasodilation is minimal with the phenylalkylamines, the major mechanism of action is causing negative inotropy. Phenylalkylamines are thought to access calcium channels from the intracellular side, although the evidence is somewhat mixed.

Verapamil does not contribute much to vasodilation but operates as described above. Whatever the heck it means. Blessings. lance

For the 42nd time: the world is not flat!
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Interesting to note that he is saying that the primary mode of action is NOT as a vasoconstrictor but on its effect on the central nervous system. Doesn't change our appreciation of this class of meds but suggests we need to change how we think about the nature of CH.
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Handb Exp Pharmacol. 2007;(177):129-43.   


Serotonin receptor ligands: treatments of acute migraine and cluster headache.

Goadsby PJ.

Institute of Neurology, Queen Square, London WC1N 3BG, UK. peterg@ion.ucl.ac.uk

Fuelled by the development of the serotonin 5-HT(1B/1D) receptor agonists, the triptans, the last 15 years has seen an explosion of interest in the treatment of acute migraine and cluster headache. Sumatriptan was the first of these agonists, and it launched a wave of therapeutic advances. These medicines are effective and safe. Triptans were developed as cranial vasoconstrictors to mimic the desirable effects of serotonin, while avoiding its side-effects. IT HAS SUBSEQUENTLY BEEN SHOWN THAT THE TRIPTANS' MAJOR ACTION IS NEURONAL, WITH BOTH PERIPHERAL AND CENTRAL TRIGEMINAL INHIBITORY EFFECTS, AS WELL AS ACTIONS IN THE THALAMUS AND AT CENTRAL MODULATORY SITES, SUCH AS THE PERIAQUEDUCTAL GREY MATTER. Further refinements may be possible as the 5-HT(1D) and 5-HT(1F) receptor agonists are explored. Serotonin receptor pharmacology has contributed much to the better management of patients with primary headache disorders.

PMID: 17087122 [PubMed]
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J Clin Neurosci. 2010 Mar 11.

What has functional neuroimaging done for primary headache ... and for the clinical neurologist?
Sprenger T, Goadsby PJ.

UCSF Headache Centre, Department of Neurology, University of California, 1701 Divisadero St, Suite 480, San Francisco, CA 94115, USA.

Our understanding of mechanisms involved in primary headache syndromes has been substantially advanced using functional neuroimaging.

THE DATA HAVE HELPED ESTABLISH THE NOW-PREVAILING VIEW OF PRIMARY HEADACHE SYNDROMES, SUCH AS MIGRAINE AND CLUSTER HEADACHE, AS BRAIN DISORDERS WITH NEUROVASCULAR MANIFESTATIONS, NOT AS DISORDERS OF BLOOD VESSELS.

PMID: 20227279 [PubMed]

Which is a technical way of saying the more we learn about these damned things the less it seems we know! ;)

Joe

Guiseppi wrote on Sep 12^th, 2011 at 10:57am:

Which is a technical way of saying the more we learn about these damned things the less it seems we know! ;) Joe

Is that like saying the fasterer I go the behinderer I get? :D