Migraine treatment

[iBS1972]

The pathophysiology of migraines is still controversial with two or three predominant theories. Vasodilation of perivascular sensory afferents is thought to be the key to the pain portion of the migraines. This makes sense as some of the termination medications are triptans which vasoconstricts vessels. However, I don't understand why beta-blockers and calcium channel blockers are used as preventative medications, since they cause vasodilation, particularly calcium channel blockers. Could someone explain this please? Thanks in advance.

Edit: Vasodilation triggers perivascular sensory afferents.

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[shisong]

I thought beta channels induce vasodilations so if you block that you will induce vasoconstriction

 

[iBS1972]

I thought beta channels induce vasodilations so if you block that you will induce vasoconstriction

You're right Beta blockers will cause vasoconstriction, but what about calcium-channel blockers? That was actually the one I was more confused about.

 

[Stagg737]

You're right Beta blockers will cause vasoconstriction, but what about calcium-channel blockers? That was actually the one I was more confused about.

There's different theories, but from what I remember the one we were taught as the predominant one is that there is an initial vasoconstriction in migraine episodes leading to hypoxemia/ischemia and the painful portion of the migraine is due to the vessels re-dilating after the initial episode of constriction. By using Ca-channel blockers prophylactically, the initial vasoconstriction doesn't occur (cerebral vessels remain dilated) which prevents the migraines. The actual pathophys isn't well understood, and I may be wrong in my explanation, but I remember that being one of the theories that was presented to us and it seems to at least make sense logically.

 

[iBS1972]

Thanks Stagg, that makes a lot of sense!