Written by admin on 2009-03-11T12:57:35+0000">March 11, 2009 – 12:57 pm
We really don’t know what causes migraine. Some doctors think that it is related to abnormalities in the workings of the nervous tissue in the brain; others think that it is mainly due to changes in the blood supply to the brain caused by the irritability and instability of the arteries themselves. The final answer, of course, may well be a bit of each – partly nervous, partly vascular.
One of the first theories about migraine was that it was due to changes in blood vessels in the head: those on the outside are dilated; those on the inside constricted. This would explain what happens in the visual aura. The way that the flickering (and particularly expanding) zig-zags of light occur in the visual aura is easy to explain if there is some sort of abnormal effect happening to the nerve cells in the visual cortex, spreading out rather like a ripple from a stone thrown into a pond. If a wave of blood-vessel contraction were to spread out from a central point in the visual cortex at about three millimetres per minute, it would produce exactly the effect migraineurs observe in the aura.
Each visual cortex (where visual information is processed in the brain) deals with visual information from one side, not one eye, so the flickering and blind spots seem to occur in both eyes together not because the eyes are affected, but because the areaj processing the information is sending off signals that are confusingly not genuine.
The aura can be aborted by using drugs that open up the arteries in the brain. However, most migraines occur without an aura, so how do they fit in? In addition, the way the aura spreads doesn’t correspond to the distribution of blood vessels in the brain. It seems to go across boundaries between blood vessels without stopping – not what you’d expect if it were the constriction of blood vessels that starts off the whole process.
The next theory states that it’s not the blood vessels that go wrong, but the nerves, and that blood-vessel changes are secondary. This would explain why the visual disturbances of the aura come before the headache. The prodromal symptoms – such as euphoria, food cravings and increased appetite – could be due to abnormal activity in a part of the brain called the hypothalamus (a region of the brain with nerve connections to most other parts of the nervous system).
A third theoiy is that those things that trigger migraine interfere chemically with the blood, creating abnormal levels of a chemical called 5-HT. We’ve known for a long time that 5-HT levels change during a migraine attack, and an injection of 5-HT can abort migraines. 5-HT-depleting drugs can increase the number of migraines in susceptible people. Most of the 5-HT in the blood is in the platelets, which are the tiny cell-like structures responsible for initiating clotting.
5-HT has effects on the blood vessels; and the lower parts of the brain are rich in nerves which use 5-HT as their transmitter chemicals. These nerves connect extensively with the higher parts of the brain, so a disturbance of these could well trigger off events higher up in the brain. Another theory involves the trigeminal nerve, which senses pain across the side of the face. When this is stimulated it causes blood vessels outside the brain Iq open up, and the suggestion is that the spreading wave of depression of the nerve-cell activity finally hits the part of the brain where the trigeminal nerve terminates, causing it firstly to give off pain signals, and secondly to cause blood-vessel enlargement.
Magnesium in the brain has recently attracted a lot of attention. During an attack magnesium levels seem to be low in migraine patients. Magnesium is important in controlling the contraction of blood vessels, as well as controlling the release of transmitter chemicals that send messages from nerve to nerve in the brain. It is also connected with platelet stickiness and clumping may well have a part to play.
Yet another theory involves (he stellate ganglion. If the stellate ganglion doesn’t work properly, it sends nerve signals which make the arteries go into spasm. The brain can’t function without blood, so it over-rides this contraction, opening up the arteries in the brain, and increasing the blood-pressure inside the skull and brain. This theory would also explain why women are more susceptible to migraines, because the female hormones cause more fluid to accumulate in the region around the stellate ganglion causing it to function less well (through oedema). Any damage to the neck or spine in the past can later cause spasm in the area which would affect the function of the stellate ganglion.
Explanations for the pain of migraine are just as confusing. At first, it looked as though the headache was due to pain in the blood vessels outside the brain, especially because of its throbbing nature, beating in time with the pulse. Reducing the pressure reduces the headache – but only in about one-third of all patients.
So what is the answer? It may well be an amalgamation of bits from each theory. There is a Unifying theory, which tries to pull all these disparate pieces of evidence together; but for the moment the answer is that we really don’t know for sure.
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