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A higher frequency of hypoplasic vertebral artery (VA) in patients with migraine with aura than in normal controls has been documented. However, the role of a hypoplasic VA in a migraine attack remains unclear. The aim of our work was to measure the net VA flow volume and related spectral parameters in patients with migraine with aura and a hypoplasic VA. From January 2005 to October 2005 we reviewed the records of 250 migraine outpatients (108 men and 142 women; mean age = 30.8 ± 14.0 years, range = 25–55). Ninety-two patients with migraine with aura were selected. Among these patients, 26 had a hypoplasic VA that was delineated by cervical magnetic resonance angiography. We performed a case-control study that included these 26 migrainous patients. Duplex color-coded ultrasonography was utilized to calculate the spectral parameters during attacks and headache-free periods. The net VA flow volume did not decrease during attacks. A reduction in the resistance index of the hypoplasic VA was noted during attacks in subjects who had migraine with aura. Our observation of VA vasomotor alteration during migraine attacks extends the understanding of the role of a hypoplasic VA. Vasomotor regulation of the VA could be neurogenic in origin. We hypothesize that VA hypoplasia contributes to migraine through complex neurovascular pathways rather than through its low flow volume. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Anterior cerebral artery A1 segment hypoplasia is an uncommon fetal variant of the circle of Willis. The frequency of this congenital variation is 1–13% as derived from angiograms and autopsy reports. Impaired collateral blood flow through the circle of Willis is a recognized risk factor for ischemic stroke. The A1 segment of the anterior cerebral artery is a principal supplier of anterior collateral blood flow. The aim of our study was to determine whether A1 segment hypoplasia may be responsible for acute ischemic stroke. We consecutively examined 280 acute ischemic stroke patients (aged 66.9 ± 14.2 years). Cerebral magnetic resonance angiography was performed within 72 h of ischemic stroke onset. The overall incidence of A1 variation in our experimental group was 15.0% (n = 42, agenesis/hypoplasia = 18/24), which was statistically higher than in the control group (n = 12). The majority (n = 30, 71.42%) had ipsilateral striatal lacunar infarctions. Based on our results, A1 agenesis/hypoplasia appears to be a risk factor contributing to ischemic stroke, especially to strokes in arteries penetrating the striatal area. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]