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What happens to the brain during M attack...

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What happens to the brain during M attack... Empty What happens to the brain during M attack...

Post  Cluelesskitty Mon 18 Apr 2011, 4:46 pm

Interesting text that may shed a bit of light what happens to us at various stages of M:

http://www.migrainesurvival.com/understand-migraine-pathophysiology-allodynia

looks like 2+2 not always obviously = 4

We know that there are waves of electrical changes that go across the brain, starting at the back and moving slowly towards the front. First there is a wave of excitation, followed by what is called spreading cortical depression. This has been known since the 1940s, when it was discovered in rabbits by a Brazilian neurologist named Leao, although it wasn’t immediately associated with migraine at that time

(hmmmm. somebody screwed that one up, didn't he?)


We have since made an association between cortical spreading depression and migraine aura.

(whew!!!)

There is also evidence of brainstem activation at the beginning of a migraine. Areas of the brainstem show up as brightly active on PET scans in the beginning of a migraine attack. These studies have indicated that brainstem activation occurs in both migraine with and without aura.

Based on research, the best understanding we now have is that migraine arises from abnormally excitable neurons in the brain and trigeminal nerve. What causes the neurons to be abnormally excitable? Various things can do this, including low magnesium, abnormal calcium channels on the surface of the neuron, mitochondrial abnormalities, or other inherited brain chemical abnormalities. The newest things in the migraine story are the glia—the support cells in the brain—which also appear to have a role in transmitting pain, perhaps moreso in chronic headache, although their story is still being determined.

According to existing trigeminovascular theory, once the messages come from the activated cells in the trigeminal nucleus in the brainstem, and travel to the trigeminal nerves that go to the dural blood vessels on the brain’s surface, it causes dilation. It also causes the release of brain chemicals called neuropeptides (substance P, CGRP or calcitonin gene-related peptide, neurokinin A, 5HT or serotonin, and noradrenalin.)



The release of these chemicals causes inflammation, and what is called peripheral sensitization. This is most likely what results in the throbbing pain most people experience. As the attack progresses, something can occur called central sensitization. When this occurs, it causes what is known as cutaneous allodynia. This means that things that are usually just a normal touch are now felt as painful. Many headache patients with allodynia cannot continue to wear earrings, necklaces or neckties, or their glasses. Some find that they cannot lie down on the side of the head pain, or report that “even their hair hurts.” Up to 80% of migraine sufferers are affected by some degree of cutaneous allodynia, and it generally occurs in the late stages of a migraine attack when the pain is severe. This is why it is important to treat early when the pain is mild or moderate
.

Risa
Cluelesskitty
Cluelesskitty
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