[Cerebral blood flow in migraine without aura].
For several years, cerebral blood flow (CBF) studies have been fueling the controversy surrounding the pathophysiology of migraine headache. The earliest studies focused mainly on migraine with aura (MA+) and provided evidence in support of the classical hemodynamic theory: a decrease in blood flow during the aura is followed by reactive vasodilation during the headache phase. Studies in migraine without aura (MA-), although less numerous, consistently demonstrated an increase in CBF during the attack. Olesen et al., gave rise to a heated debate by suggesting that hemodynamic manifestations are different in MA+ and MA-; in their view, CBF remains unchanged in MA-, whereas MA+ is associated with a wave of posterior blood flow deficiency which slowly spreads forwards in a manner reminiscent of experimental spreading depression; they interpret this hemodynamic pattern as evidence that the attack is mainly caused by a neural mechanism rather than a vascular spasm. This concept of MA- with no hemodynamic changes suggests that the pathophysiology of MA- may be completely different from that of MA+. However, most studies using stationary detectors or single photon emission computerized tomography (SPECT) with Xenon 133 or HMPAO as the tracer have demonstrated increased CBF during migraine attacks. The increase was not correlated with the side of the pain suggesting that vasodilatation is not the only cause of the pain. Current data do not seem to support the view that MA- and MA+ are different pathophysiologic entities; whether the mechanism of the attack is neural or vascular cannot be determined on the basis of CBF data.(ABSTRACT TRUNCATED AT 250 WORDS)