The classical medical model of primary headache essentially contains 3 “groups”.
The first of these are “Tension Headaches”, the second is “Migraines” and the third group contains such headaches as Cluster, SUNCT and Chronic Paroxysmal Hemicrania.
This classical medical model considers that the cause of Migraines are likely to be related to a dilation of blood vessels in the brain. However, is this really the case? There is significant medical research over the past 15 years that give us reason to seriously doubt that an increase in blood vessel dilation in the brain is the cause of Migraines.
The research shows:
- Dilation of blood vessels does not necessarily coincide with pain. If dilation of the blood vessels in the brain was indeed the cause of migraines, it stands to reason that when they dilate, pain of the migraine would come on and when they constrict, pain reduce. However, this is clearly not the case.
- Dilation of blood vessels is the consequence of head pain, not the cause.
- Not all migraine sufferers have dilation of blood vessels in the brain during their headache. There is evidence to suggest that many sufferers of Migraine get either no change to the blood vessels and in some cases a constriction of blood vessels in the brain during their headache. If dilation of blood vessels is indeed the cause of migraine, shouldn’t all migraine sufferers get a dilation of the brain’s blood vessels during a headache?
- The magnitude of dilation is thought to be about 9%. Is this too small a change to cause migraine? Maybe, maybe not, but it is a really small change isn’t it?
At a recent headache seminar I attended, the presenter (Mr Dean Watson – MAppSc (Research – Manipulative Physiotherapy) and Consultant Headache and Migraine Physiotherapist, PhD Candidate) quoted research on Migraines that said:
“It cannot be excluded that noxious events in and around other pain sensitive structures, both extra and intracranially may contribute in addition” (Thomsen, 1997)
This essentially means that other structures, either in or outside the head (like the neck) are being considered as alternative sources or contributers to the pain of Migraines. The same researcher goes on to state in his study:
“…….that a possible mechanism of sensitisation to noxious inputs could be via heightened nociceptive sensitivity in the central nervous system” (Thomsen, 1997)
This poses the question that maybe the nerves that carry the “pain” message from the pain producing structures that are located in or outside the head to the brain are somehow sensitized. That is, a small change in intensity or mechanical stimulus causes a large response. Think about what happens when you talk into a microphone. Even a small whisper can be audible over a wide area. A small input, LARGE output.
This opens up the possibility that if we can desensitize these structures, maybe we can actually reduce the pain of Migraine.
Food for thought?