Medical What Are the Four Phases of a Migraine Episode?

[waht]

how has this been diagnosed as a result of a migraine episode? Is it because the person experienced a lot of migraines accompanied by headaches before?

 

[zoobyshoe]

how has this been diagnosed as a result of a migraine episode? Is it because the person experienced a lot of migraines accompanied by headaches before?

The article linked to in the OP lists common migraine auras:

# visual symptoms: flashing lights, wavy lines, spots, partial loss of sight, blurry vision
# olfactory hallucinations (smelling odors that aren't there)
# tingling or numbness of the face or extremities on the side where the headache develops.
# difficult finding words and/or speaking
# confusion
# vertigo
# partial paralysis
# auditory hallucinations
# decrease in or loss of hearing
# reduced sensation
# hypersensitivity to feel and touch

Anyone presenting with one of these symptoms would be put through a differential diagnosis by the neurologist. Any given symptom might be associated with, say, 5 different conditions. Each of those conditions, though, has other symptoms included in their sine qua non. When those other symptoms are not present that other condition can be excluded.

The list of suspects might then be reduced to say, three possible diseases. There might be tests for two of them. Testing positive for one of the two indicates that is the culprit. Testing positive for neither points the finger at the third. Treatment would be started for the most likely culprit, and the patient monitored. If the treatment works, the diagnosis would be considered accurate. If the treatment doesn't have the expected results, everything has to be reconsidered.

This procedure is carried to the extreme on just about every episode of House if you have ever had the chance to see that television program.

 

[zoobyshoe]

Unusual Migrain Aura - Personal Account by Oliver Sacks

I find it to be exceptionally fortunate for anyone interested in learning about migraine that Neurologist Oliver Sacks, who is the foremost writer of popular literature on neurology, suffers from migraine himself, and also spent many years as a specialist at a clinic for migraine. His abilities as a writer, his personal and clinical experiences, and his professional training put him in a unique position to understand and articulate the condition:

While visual auras are the commonest, there may be other types. There are sometimes auditory auras in which sounds seem abnormally loud, soft, or distorted; one may hear hallucinatory tunes, as Hilary Mantel describes in her book; one may lose all sense of pitch and tone, or become unable to recognize (normally) familiar music. I have twice had such “amusic” migraine auras myself, and I have described them recently in “Musicophilia.” Here is the passage from the book:

I experienced amusia myself on two occasions, both in 1974. On the first, I was driving along the Bronx River Parkway, listening to a Chopin ballade on the radio, when a strange alteration of the music occurred. The beautiful piano tones started to lose their pitch and their character and were reduced, within a couple of minutes, to a sort of toneless banging with an unpleasant metallic reverberation, as if the ballade were being played with a hammer on sheet metal. Though I had lost all sense of melody, I had no impairment of rhythmic structure. A few minutes later, just as the piece was ending, normal tonality returned. Greatly puzzled by all of this, when I got home I phoned the radio station and asked them if this had been some sort of experiment or joke. They said no, of course not, and suggested that I get my radio checked.

A few weeks later I had a similar episode while playing a Chopin mazurka on my piano. There was again a profound loss of tone, and the music seemed to decompose into a disconcerting racket, along with an unpleasant metallic reverberation. But this time it was accompanied by a brilliant, scintillating zigzag expanding in half of my visual field—I had often experienced such zigzags during attacks of migraine. Now, it was evident, I was experiencing an amusia as part of a migraine aura. Still, when I went downstairs and spoke to my landlord, I found that my voice and his voice sounded perfectly normal. It was only music, and not speech or sound in general, that was so strangely affected.

http://migraine.blogs.nytimes.com/2008/02/26/answers-to-reader-questions/

 

[Moonbear]

I get migraines with changes in weather (there was actually an article out on this recently confirming that weather changes can cause migraines...I was surprised nobody had figured that out sooner), and had one that lasted two days this week through a combination of weather and menstrual symptoms (those are the real killer headaches, when both triggers coincide). Ugh! I don't always get the olfactory symptoms, but this time I did...kept swearing I was smelling cigarette smoke, even in my own house where nobody is ever allowed to smoke. I also get a weird, hazy feeling starting a few hours before the headache itself kicks in.

What's interesting is that I know of plenty of people who just call any headache a migraine and don't know the difference, but an ENT gave a talk recently, and mentioned that he sees a lot of patients who think they are getting sinus headaches and when he checks them out, they have perfectly clear sinuses, and it'll turn out that they are getting migraines with the pain mostly localizing around the sinuses.

 

[zoobyshoe]

I get migraines with changes in weather (there was actually an article out on this recently confirming that weather changes can cause migraines...I was surprised nobody had figured that out sooner), and had one that lasted two days this week through a combination of weather and menstrual symptoms (those are the real killer headaches, when both triggers coincide). Ugh! I don't always get the olfactory symptoms, but this time I did...kept swearing I was smelling cigarette smoke, even in my own house where nobody is ever allowed to smoke. I also get a weird, hazy feeling starting a few hours before the headache itself kicks in.

What's interesting is that I know of plenty of people who just call any headache a migraine and don't know the difference, but an ENT gave a talk recently, and mentioned that he sees a lot of patients who think they are getting sinus headaches and when he checks them out, they have perfectly clear sinuses, and it'll turn out that they are getting migraines with the pain mostly localizing around the sinuses.

Since you are a neuroscientist and also suffer from migraine I'm sure you'll be interested in the phenomenon of Cortical Spreading Depression , which has been at the center of most Migraine research for a couple decades now, but which isn't very often mentioned in popular literature for Migraineurs:

Pathophysiology of the migraine aura. The spreading depression theory.

Lauritzen M.

Laboratory of Clinical Neurophysiology, Rigshospitalet, Copenhagen, Denmark.

The characteristic form and development of sensory disturbances during migraine auras suggests that the underlying mechanism is a disturbance of the cerebral cortex, probably the cortical spreading depression (CSD) of Leão. The demonstration of unique changes of brain blood flow during attacks of migraine with aura, which have been replicated in animal experiments during CSD, constitutes another important line of support for the 'spreading depression' theory, which may be a key to an understanding of the migraine attack. Cortical spreading depression is a short-lasting depolarization wave that moves across the cortex at a rate of 3-5 mm/min. A brief phase of excitation heralds the reaction which is immediately followed by prolonged nerve cell depression synchronously with a dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells and enhanced energy metabolism. Recent experimental work has shown that CSD in the neocortex of a variety of species including man is dependent on activation of a single receptor, the N-methyl-D-aspartate receptor, one of the three subtypes of glutamate receptors. The combined experimental and clinical studies point to fruitful areas in which to look for migraine treatments of the future and provide a framework within which important aspects of the migraine attack can be modeled.

http://www.ncbi.nlm.nih.gov/pubmed/7908596?dopt=Abstract

This is primarily linked to the visual aura, but probably also explains other auras, such as yours, when it happens in other brain regions.

There is a lot of debate about how the CSP might be linked to the pain. Hyperexitability of the neurons of Migraineurs has been demonstrated with Transcranial Magnetic Stimulation, and that was suggested as the underlying cause of Migraine, but the most interesting abstract to catch my attention was one in which it's asserted that malformations or variants of the arterial circle of willis best explains all manifestations of the condition:

Migraine and circle of Willis anomalies.

Cucchiara B, Detre J.

Department of Neurology, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, PA 19104, United States. cucchiar@mail.med.upenn.edu

Several mechanisms are currently thought to contribute to migraine pathogenesis, including interictal neuronal hyperexcitability, cortical spreading depression underlying the symptom of aura, and trigeminal nerve activation at a peripheral and central level. However, these mechanistic concepts incompletely explain migraine susceptibility in individual patients and do not fully account for the well documented association between migraine and ischemic cerebrovascular disease, including increased risk of both clinical stroke and subclinical brain lesions in migraine patients. The circle of Willis is a major source of collateral blood flow supply in the human brain, and developmental morphologic variants of the circle of Willis are extremely frequent. Altered cerebral blood flow (CBF) has been demonstrated in regions supplied by variant circle of Willis vessels. 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. Identification of structural alterations in the cerebral vasculature in migraine patients would have several important pathophysiological and clinical implications. First, it would provide a developmental mechanism for migraine susceptibility that may lead to further insights into genetic predisposition to migraine. Second, it would expand understanding of potential mechanisms underlying migraine aura and linking migraine with both clinical and subclinical cerebral infarction. Third, it could help to identify the subpopulation of patients at risk of progressive cerebral ischemia so as to target preventative therapies appropriately. Fourth, it would suggest a role for further diagnostic evaluation to determine migraine mechanism in individual patients, analogous to the current paradigm in ischemic stroke in which determination of stroke mechanism is critical to therapeutic decision-making.

PMID: 18226467 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/18226467?dopt=Abstract

As it says, "developmental morphologic variants of the circle of Willis are extremely frequent". I googled and found that this is, in fact the case, and that it's quite possible to be born with an incomplete circle of willis, or a grossly varied one, and that suggests to me that the genetic predisposition to a willis variant is the genetic "cause" of migraine.

The circle of willis hypothesis was also extremely exiting to me because ischemia is a well know seizure trigger and this would strongly point to willis variations as the reason for the unusually high cormorbidity of seizures and migraine, and also, therefore, could explain why predisposition to seizures tends to run in some families. I hope migraine and seizure researchers notice that paper and that people start collecting images of the circle of willis of migraineurs and idiopathic seizure sufferers to see if there's a high incidence of variant ones.

In the meantime, here's a link to a massive page of abstracts on Cortical Spreading Depression many of which go deep into chemical activities that you are in a position to fathom:

http://neurotransmitter.net/migrainecsd.html

 

[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.