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Cerebral Hypoperfusion Followed by Hyperperfusion in Classic Migraine-Reply

Allan Renard Andersen, MD; Jes Olesen, MD; Tom Skyhø Olsen, MD; Lars Friberg, MD
Arch Neurol. 1989;46(6):606-606. doi:10.1001/archneur.1989.00520420024015
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In Reply.  —We appreciate the comments from Vijayan and from Spierings and Graham to our recent article in the Archives.1 They rightly point to the possible importance of arterial mechanisms, in particular outside of the brain, for pain production during migraine attacks. The earlier conclusions by Wolff's group were based on methodology that today must be regarded as unreliable and due consideration was not given to control groups and statistical evaluation. While the potential for study of cerebral blood flow has greatly increased over recent years, the same, unfortunately, is not true of our possibilities to study arterial diameter and pulsations intracranially and extracranially. Our study has ruled out certain pain mechanisms, but not the possibility that pain is due to abnormalities in and around arteries. This is a topic for future research and the problems may possibly be dealt with by newly developed ultrasound equipment. It might be worthwhile to

REFERENCES

Andersen AR, Friberg L, Skyhø Olsen T, Olesen J.  Delayed hyperemia following hypoperfusion in classic migraine . Arch Neurol . 1988;;45:154-159.
Jensen K, Olesen J.  Temporal muscle blood flow in common migraine . Acta Neurol . 1985;;72:561-570.
Jensen K.  Subcutaneous blood flow in the temporal region of migraine patients . Acta Neurol . 1987;;75:310-318.

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Andersen AR, Friberg L, Skyhø Olsen T, Olesen J.  Delayed hyperemia following hypoperfusion in classic migraine . Arch Neurol . 1988;;45:154-159.
Jensen K, Olesen J.  Temporal muscle blood flow in common migraine . Acta Neurol . 1985;;72:561-570.
Jensen K.  Subcutaneous blood flow in the temporal region of migraine patients . Acta Neurol . 1987;;75:310-318.

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