Blood Vessels and Migraine

The medical model of headache and migraine recognizes two conditions – migraine and tension-type headache. Recently the International Headache Society introduced a third ‘group’ of headaches; this group comprises Cluster Headache, Chronic Paroxysmal Hemicrania, SUNCT, and Hemicrania Continua.

In this model, the pain of migraine is considered to be from dilating or expanding arteries inside the head – an assumption based largely on the nature of pain – a throbbing, pulsating pain.

However research has shown:

Blood vessel dilatation persists after head pain has resolved – if dilatation were the cause of the pain one would expect pain to be there if dilatation was present, but this is not the case.

Blood vessel dilatation is not present in all migraineurs during an attack – if it was the cause one would expect it to be present in all sufferers.

Blood vessel dilatation is estimated to be about nine percent – too small to cause the significant pain of migraine?

Pain leads to or causes dilatation, not dilatation first, followed by pain.

Clearly this body of research demonstrates that dilatation of arteries is not the cause of migraine pain – why is it then that some authorities and information sources perpetuate this assumption?

Cheers

Dean

(Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders, 2nd edn. Cephalalgia 2004; 24(suppl.1):1-151

Tegeler CH, Davidai G, Gengo FM, Knappertz VA,Troost BT, Gabriel H, Davis RL. Middle cerebral artery velocity correlates with nitroglcerin-induced headache onset. J Neuroimaging 1996; 6(2): 81-6

Thomsen LL, Iverson HK, Olesen J. Cerebral bloodflow velocities are reduced during attacks of unilateral migraine without aura. Cephalalgia 1995; 15(2): 109-116

Thomsen LL. Investigations into the role of nitric oxide and the large intracranial arteries in migraine headache. Cephalalgia 1997; 17:873-95)

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