Key points are not available for this paper at this time.
The purpose of the present study was to examine the cerebral perfusion after spreading depression with special emphasis on its relation to the perfusion changes in migraine. The cerebrovascular reactivity to changes of arterial Pco 2 tension in the range of 24–70 mm Hg and to changes of MABP in the range of 55–150 mm Hg was studied in the rat brain after one episode of cortical spreading depression. Regional CBF (rCBF) was measured in the frontal, parietal, and occipital cortex, the basal ganglia, and the cerebellum of both hemispheres after the intravenous bolus injection of 14 Ciodoantipyrine. rCBF decreased in the cortical regions to 69–73% of control values for 1 h after spreading depression in every single rat, but remained unchanged in the basal ganglia and cerebellum. CBF changed with alterations of arterial carbon dioxide tension in all brain regions. In control regions, CBF changed by 2.8–3.9% per mm Hg P a co 2 change, whereas in the spreading depression cortex, CBF changed by only 1.3–1.5%. The difference between control and spreading depression cortex was significant at p < 0.001, indicating a reduced CO 2 sensitivity of the cortical regions invaded by spreading depression. rCBF remained unchanged in all brain regions in the MABP range of 80–150 mm Hg, reflecting the intact autoregulatory function of the two sides, and at a MABP of <80 mm Hg, rCBF decreased in parallel in symmetrical regions. It is concluded that the hypoperfusion after spreading depression is due to a vasoconstrictor stimulus overriding the vasodilatory effect of acid pH. The reduced CO 2 response is probably the effect and not the cause of this vasoconstriction. The coexistence of rCBF reduction with perserved autoregulation and impaired CO 2 response in an otherwise normally perfused brain has previously been found in patients during migraine attacks. This study therefore corroborates the notion that the perfusion changes of migraine may be pathophysiologically related to spreading depression and that spreading depression may serve as an experimental model of migraine.
Martin Lauritzen (Sat,) studied this question.