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The Vascular Theory Of Migraine‐Resuscitated Or More Moribund?

J. Edmeads
Published 1989 · Medicine

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Your decision to publish an important paper on cerebral blood flow (CBF) in migraine1 as the first in Headache for 1989 is to be applauded. But does it clarify or cloud the issue? After 20 years of CBF studies in migraine the results show 1) a reduction of at least 25 30% in classical migraine1, 2) an average increase of 31% in common and classical migraine2, 3) or no change in common migraine3. Now we learn that the measurements need modifying by 40% to allow for scattering of radiation the Compton scatter effect which has led to "an unbalanced interpretation of the data"1 So the results are as contradictory as they can be, the measurements require adjustment, and the interpretation is therefore doubly doubtful. From the clinical point of view the neurological aura, the enlarging scotoma, the scintillations, the migration of the paraesthesiae up the arm or visual disturbances across the visual field, have not been seen in cerebrovascular disease.4 The headache is throbbing in only 47% of 750 patients questioned during a migraine5; but even when the pain is pulsatlie, it throbs for only a portion of the time at the maximum of the headache (Blau unpublished observations). The evidence for a neurological aetiology has been examined6: the most potent argument against a vascular cause is that the common triggers stress, light and hunger go direct to the nervous system, not via blood vessels. No one denies that vascular changes occur in migraine but are they primary or secondary to a neurological disturbance? Sokoloff7 concluded that the stimulated rat and monkey cortex showed increased glucose uptake, and that the increased local blood flow occurred "in response (my italics) to changes in local functional activity". The evidence, therefore, points to an underlying neurological basis with secondary vascular responses. The vascular theory may need resuscitation but who is going to give it the kiss of life?
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