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SYNOPSIS Measurements of noninvasive regional cerebral blood flow (rCBF) were made by the 133Xe inhalation method in 71 patients with different types of headache and 32 age matched normal controls. Flow gray (Fg) was calculated by two compartmental analysis from the x‐ray subtracted gamma curves, and extracerebral flow indices (EFI) were calculated as an estimate of the percentage contribution by extracerebral tissues.During the headache phase, mean Fg in a group (N = 13) with classic and common migraine was significantly higher compared to a comparable group (N = 12) measured in the headache‐free interval. Serial measurement made during progression in the severity of the migraine headaches showed accompanying increases in the mean Fg as the headache worsened. In 24 patients with severe migraine studied 2‐48 hours after the headache subsided, the mean Fg values remained significantly increased during this immediate post‐headache interval compared with patients who were headache‐free for six days or longer. Serial measurements made during and after the headache showed progressive reduction of mean Fg values to normal within six days after the headache subsided. Marked cerebral dysauto‐regulation was present during the migraine headache and showed progressive recovery as the headache subsided. Reduction of the head pain by administration of codeine decreased hemispheric Fg values but did not change the high flows in the basilar artery territory. Conversely, administration of ergotamine did not change hemispheric Fg values but reduced rCBF in brain stem‐cerebellar regions. Significant regional reductions of Fg correlating with the neurological deficit was measured during the prodrome of classic migraine and during the headache and post‐headache intervals of complicated migraine. During cluster headaches, mean Fg values were also significantly increased and the extracerebral flow indices showed marked increases with highest values recorded at the site of the headache. It was concluded that cerebral hyperperfusion during migraine headaches is mainly due to post‐ischemic reactive hyperemia but may be compounded by functional hyperemia due to the head pain itself.
Sakai et al. (Sat,) studied this question.