Blood Flow and Vascular Reactivity During Attacks of Classic Migraine'Limitations of the Xe‐133 Intraarterial Technique

Abstract

The present study reports cerebral blood flow (CBF) measurements in 11 patients during attacks of classic migraine (CM)--migraine with aura. In 6 and 7 patients, respectively, cerebral vascular reactivity to increased blood pressure and to hypocapnia was also investigated during the CM attacks. The Xenon-133 intraarterial injection technique was used to measure CBF. In this study, based in part on previously published data, methodological limitations, in particular caused by scattered radiation (Compton scatter), are critically analysed. Based on this analysis and the results of the CBF studies it is concluded: During CM attacks CBF appears to decrease focally in the posterior part of the brain to a level around 20 ml/100 g/min which is consistent with a mild degree of ischemia. Changes of CBF in focal low flow areas are difficult to evaluate accurately with the Xe-133 technique. In most cases true CBF may change 50% or more in the low flow areas without giving rise to significantly measurable changes of CBF. This analysis suggests that the autoregulation response cannot be evaluated in the low flow areas with the technique used while the observations are compatible with the concept that a vasoconstrictive state, unresponsive to hypocapnia, prevails in the low flow areas during CM attacks. The gradual increase in size of the low flow area seen in several cases may be interpreted in two different ways. A spreading process may actually exist. However, due to Compton scatter, a gradual decrease of CBF in a territory that does not increase in size will also appear as a gradually spreading low flow area when studied with the Xe-133 intracarotid technique.

Migraine and other headaches

“…Recently, research has focused on the role of neural dysfunction in the occurrence of migraines, with reports suggesting associations with dysfunction of the sympathetic nervous system 7 and dysfunction in the brainstem related to modulation of craniovascular afferents. 9 Previous studies have reported reduced cerebral blood flow during the aura phase among those with migraine with aura 10,11 and the persistence of reduced cerebral blood flow into the pain phase of migraine. 3 Wolff's "vascular theory" suggests vasoconstriction of intracerebral ar-teries leads to ischemia and symptoms of aura and a subsequent hyperemic response leads to vasodilation and headache pain.…”

Abnormal Cerebrovascular Reactivity in Headache-Free Migraineurs

“…Studies of rCBF with intra-arterial or inhaled l33Xe have shown a quite consistent pattern of cortical oligemia in the prodromal phase of classic migraine, extending into the headache phase, followed by hyperper fusion lasting well beyond the cessation of pain [13][14][15][16][17][18]. Opinions have diverged, however, in the interpretation of the spreading oligemia of the prodromal phase.…”

“…Opinions have diverged, however, in the interpretation of the spreading oligemia of the prodromal phase. In fact, some authors view it as purely secondary to decreased neuronal function and hence reflecting a metabolic de pression of the rCBF [14,15], whereas others argue that contraction of cortical arterioles plays a crucial role and therefore true ischemia is the pathophysiological mecha nism [16][17][18].…”

Migraine With Aura: A Vicious Cycle Perpetuated by Potassium‐lnduced Vasoconstriction

“…15 Their data indicate that cerebral blood flow decreases focally to values of 20ml/100gm/min during the initial portion of the attack. Regional cortical blood flow in patients is measured most frequently using Xenon-133 washout following intravenous or intra-arterial injection of the isotope.…”