What Are the Four Phases of a Migraine Episode?

[Moonbear]

I'd have a hard time believing the Circle of Willis theory. You can pick up abnormalities of that on MRI or CT scans, and the concern of impaired flow through there would be more of a stroke risk. There are some current articles that find some variants in those vessels as a cause of neuralgias, when the vessels basically physically rub on cranial nerves and damage them. But, those types of symptoms are specific to a single cranial nerve, and occur on one side.

The other reason I'm not convinced regarding the Circle of Willis is that the reason it is a significant vascular structure is because it provides multiple levels of redundant blood flow. If you get a restriction of one part of it, blood flow can reverse direction and supply the same area from a different path. Until you get a major occlusion of a vessel, or a rupture, or an aneurysm pressing on nearby structures, abnormalities can be pretty asymptomatic.

I'll dig through the Cortical Spreading Depression stuff further. That looks more intriguing.

 

[zoobyshoe]

The other reason I'm not convinced regarding the Circle of Willis is that the reason it is a significant vascular structure is because it provides multiple levels of redundant blood flow. If you get a restriction of one part of it, blood flow can reverse direction and supply the same area from a different path. Until you get a major occlusion of a vessel, or a rupture, or an aneurysm pressing on nearby structures, abnormalities can be pretty asymptomatic.

The Circle of Willis idea is that neuronal hyperexitability (which has been demonstrated in migaineurs) plus altered blood flow (which has been demonstrated with Circle of Willis anomalies) triggers the cascade of Cortical Spreading Depression. You wouldn't need a major occlusion for an increased demand for blood to represent a relative ischemia.:

Altered cerebral blood flow (CBF) has been demonstrated in regions supplied by variant circle of Willis vessels.

In other words: the redundancy doesn't seem to lead to status quo for a normal Circles of Willis in all cases. The variants lead to "altered" CBF.

Our central hypothesis is that circle of Willis anomalies correlate with alterations in cerebral hemodynamics and contribute to migraine susceptibility and ischemic complications of migraine. Dysregulation of CBF may allow relative ischemia to develop in the setting of increased metabolic demand related to neuronal hyperexcitability, may trigger cortical spreading depression, and may predispose individuals with migraine to ischemic lesions and stroke.

Cortical Spreading Depression and Neuronal Hyperexitability alone do nothing to address the increased risk of stroke of Migraineurs. It's the very concern of increased stroke risk you mention with impaired blood flow there that further links it to Migraine. The implication is that anomalies aren't as asymptomatic as has been thought but that the symptoms only appear under certain kinds of stress on the system.

Which cranial nerve is it and which side?

I don't know if it's SOP to do scans on people presenting with Migraine symptoms, or if it is SOP if there is an effort made to specifically image and check for Circle of Willis anomalies. They may be noticed and dismissed "No big deal. A lot of people have that." kind of thing. In any event, I guess, it's up to the authors of this paper, and others interested in examining the idea, to begin collecting scans of Migraineurs to see how often Willis anomalies show up.

I'll dig through the Cortical Spreading Depression stuff further. That looks more intriguing.

That phenomenon was first inferred from the "march" of the symptoms:

The nerve cells of the brain are always active. This can be seen by the electrical activity they generate on the electroencephalogram (EEG). In experiments with animals, the EEG shows a depression (lowering) of nerve cell activity below a spot on the cortex of the brain that has been stimulated. Surrounding the area of depressed activity is a zone in which nerve cells have become hyperactive. It's thought that a similar pattern of decreased and increased nerve cell activity occurs in the brain of a person with migraine, following the stimulus of a migraine "trigger."

When the activity of nerve cells is depressed, there is impairment of function in the part of the body controlled by these cells. For example, there may be a loss of vision or of strength. Increased activity of brain nerve cells may result in flashing lights or tingling in the face and hand. In the experiments with animals, the depression of nerve cell activity slowly spreads beyond the initial spot of stimulation. This phenomenon is called spreading depression. It is preceded by a wave of increased nerve cell activity.

This slowly spreading depression of nerve cell activity is believed to account for the pattern of development of the typical aura. In the migraine aura, symptoms build up gradually and move slowly from one visual region or one part of the body to another. For example, the migraine aura sufferer may first notice a black spot in the field of vision. This black spot is often surrounded by flashing lights or bright zig-zag lines. The size of the black spot gradually enlarges over a period of minutes. The combination of loss of vision (negative symptoms) with flashing lights or zig-zag lines (positive symptoms) is a typical and distinctive feature of migraine aura. The negative symptom (blacking out of vision) is due to depressed nerve activity; the positive visual symptoms are due to the zone of hyperactive nerve cells. In contrast, a sudden shutting off of blood supply to the brain (as might occur with a blood clot) causes a sudden loss of function. In this case, there is no gradual "march" of visual symptoms or numbness, and positive visual symptoms do not occur.

http://headaches.about.com/od/migrainediseas1/a/aura_ache.htm

The significance of the "March" is that it demonstrates that the activity responsible for the symptoms is starting in one place in the cortex and very slowly expanding out into all the surrounding cells, whatever we suppose the specifics of that activity to be. The concept of the Migraine aura as a spreading slow "wave" of neuronal activity is apparently extremely old. Oliver Sacks, born in 1933, heard it from his mother at the age of three or four, which sets the year of this anecdote as 1936-1938:

I have had migraines for most of my life; the first attack I remember occurred when I was 3 or 4 years old. I was playing in the garden when a brilliant, shimmering light appeared to my left — dazzlingly bright, almost as bright as the sun. It expanded, becoming an enormous shimmering semicircle stretching from the ground to the sky, with sharp zigzagging borders and brilliant blue and orange colors. Then, behind the brightness, came a blindness, an emptiness in my field of vision, and soon I could see almost nothing on my left side. I was terrified — what was happening? My sight returned to normal in a few minutes, but these were the longest minutes I had ever experienced.

I told my mother what had happened, and she explained to me that what I had had was a migraine — she was a doctor, and she, too, was a migraineur. It was a “visual migraine,” she said, or a migraine “aura.” The zigzag shape, she would later tell me, resembled that of medieval forts, and was sometimes called a “fortification pattern.” Many people, she explained, would get a terrible headache after seeing such a “fortification” — but, if I were lucky, I would be one of those who got only the aura, without the headache.

I was lucky here, and lucky, too, to have a mother who could reassure me that everything would be back to normal within a few minutes, and with whom, as I got older, I could share my migraine experiences. She explained that auras like mine were due to a sort of disturbance like a wave passing across the visual parts of the brain. A similar “wave” might pass over other parts of the brain, she said, so one might get a strange feeling on one side of the body, or experience a funny smell, or find oneself temporarily unable to speak. A migraine might affect one’s perception of color, or depth, or movement, might make the whole visual world unintelligible for a few minutes. Then, if one were unlucky, the rest of the migraine might follow: violent headaches, often on one side, vomiting, painful sensitivity to light and noise, abdominal disturbances, and a host of other symptoms.

http://migraine.blogs.nytimes.com/2008/02/13/patterns/

Spreading Depression, discovered by a researcher named Leao in 1944, but not linked to anything in particular by him, was eventually noticed to have all the right dynamics to explain the "march" of the visual aura in Migraine. It has been picked up by magnetoencephalography in Migraineurs whose auras were artificially triggered by visual stimulation:

http://www.springerlink.com/content/bnwj3fb82pu679kq/

And it has been picked up in all kinds of animal studies when artificially stimulated. Most neurologists seem to be persuaded that CSD is the likely mechanism of the aura (not the headache, or the condition of Migraine in general, just the aura).

 

[zoobyshoe]

I would actually like to see it again, it was that fascinating.

In his book, Migraine, Sacks says the scintillating scotoma may be triggered by flickering light. He says it seems only to work in the case of flickering between 8 and 12 times a second. It's the frequency, according to him, that's critical, not that it be light, because sound at the same frequency also seems to trigger the scotoma. He cites jackhammers as having the same effect.

Here at this page:

http://www.boston.com/bostonglobe/ideas/graphics/011109_hacking_your_brain/

the last two panels in the bottom row describe something quick and dirty you might try to see if you can trigger a scotoma. I don't reccomend this, and I wouldn't try it unless you have time to go through the whole cycle of the scotoma in case it works.