Confusing question from ignorance

From the “This Is Going to Sound Really Dopey, and You Could Probably Say ‘You Could Ask the Same Question About ANY Disorder / Disease in the World’ but I’m Curious Nonetheless” Department [a subsidiary of the People Against Wordy Subheaders Group]:

We’ve got all sorts of medicines flying around for MAV prophylaxis – calcium-channel blockers, beta-blockers, SSRI’s/SNRI’s (antidepressants), anticonvulsants, antihypertensives … the list goes on! Yet one medicine completely works for one person, yet others, the same pill doesn’t do a darned thing. Some people have to trial-and-error their way into a veritable cocktail of drugs.

So here’s what I’d like to know. Are there different forms of MAV – or at least, different causes? Or are they all believed to ultimately have the same origin? (I do know, of course, that migraines themselves have a variety of causes, but MAV isn’t as clear.)

All the medicines, like the ones above, have completely different mechanisms of action. Is there a “bigger picture” that science as a whole is missing? It almost seems as though there’s some fundamental “thing” nobody’s discovered yet that underlies the entire realm of migraines and MAV.

Especially with the dizziness/vertigo component. Does the cause of that precise problem (the dizziness) vary from one MAV sufferer to another? Or is there perhaps some underlying mechanism and nobody’s figured out yet how it really works?

It’s all just confusing to me, insofar as there’s no telling which family of medicine will be the one that does the trick. For some, it’s the SSRI’s; for others, it’s beta-blockers.

… Sure, I COULD ask all this to Dr. Hain when I see him next. I’m sure he has three-plus hours to explain all this to a layman like me, ha. Anyway, if anyone would like to comment on any or all of this (including “your posts are too long”), I’d be interested.

Great questions. Unfortunately, I don’t believe anyone has the answers yet, including Dr. Hain.

Hi George,

Really good question. I doubt anyone really has a good answer either. All I can come up with is to follow on from what Carolyn Bernstein says about “migraine brains” in that they are all slightly different. So maybe it’s a combination of the areas in the brain that are most impacted by migraine and also to do with someone’s genetic make-up. So depending on how your brain is wired and the sorts of receptors (made up of proteins) that exist might explain why a drug such as propranolol works for one person and not another.

I’m thinking about putting together a “top 10 MAV questions” and sending it off to Dr Rauch for comment. I think he’ll answer them for us. Your Q will be in the list.

Scott 8)

Only problem with that is, my “question” was about five different queries all entangled within one another!

I have a couple of suspicions about the answer, but nothing particularly insightful.

It seems that the closest thing we have to a common thread (in migrainous vertigo) is the role of neurotransmitters and neuropeptides. Well, maybe that’s not entirely accurate. However, given what info there is about the “migraine circuit,” it sounds quite possible, at least to me.

Actually, one of the theories I have about this is that the longer the MAV “endless loop” goes on (e.g., how long a person has had the vertigo), the more complex of a process it becomes and thus the more difficult it is to stop. What’s more, they say migraines change form, right? That doesn’t necessarily mean the change is only in how we EXPERIENCE them – perhaps there’s a fundamental shift in the process, and it CAUSES migraines to change form. Migraines don’t just “decide” one morning, “You know, I’m tired of being a headache. I think I’ll make Bob sick and woozy, instead.” That is to say … if migraines change form, which we know they do, there has to be something that’s RESPONSIBLE for the change. It can’t just be a random process. The brain doesn’t work like that.

In a slightly tangential vein, I’d compare this to “breaking a bad habit” – the longer one’s been doing (X habit), the harder it is to break. Perhaps MAV reaches certain points or thresholds at which new chemicals, and/or new parts of the brain, gradually become “drawn in” into the cycle and thus require progressively stronger medicines – ones that attack on multiple fronts, e.g., both the calcium channel and the serotonin/norepinephrine levels.

… See, this is why I should keep my mouth shut and let the EXPERTS figure out the answers … I clearly don’t have a coherent thought in my head on the matter! (What do you do for an encore, George – go and try to propose new physics theories to NASA scientists?)

Hi George,
I’ve asked myself the same questions, why are we all so different?
Jenny’s theory which isn’t really true and holds no weight anyway, is: :mrgreen:

We all have different areas of the brain where the vessels become constricted and cortical spreading depression strikes, so different parts of our brain and vestibular system are attacked during a migraine.
Not everyone’s brain is assaulted in the same part of the brain, of cause with mav, it’s attacking the motor functions and coordination parts of the brain and vestibular system, for people with aura it is also attacking the visaul cortex or eyes. ect…

Every one has different symptoms probably because of where the cortical spreading eventual settles or spreads or is sitting in that part of the nerves or cells.
Another person might have “Aphasia”with migraine, then the attack is in the area of the speech and language banks or memory banks for language.

About aphasia:

I know I have aphasia and also have trouble deciphering language or the written word during a migraine.

People with epilepsy have varying types, so do migraineurs. I think epilepsy is very similar to a migrainous event but much less invasive to the brain.
My migraines have always been similar to a simple partial seizure.
So yes we are all different and have differing symptoms.

So yes this is my theory, not a good one but I don’t mind.
I’m in a good place today and am happy to ramble on for you.
Also what was your question George? :oops:

Jen xx