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. 2010 Nov 3;31(1):17–35. doi: 10.1038/jcbfm.2010.191

Figure 1.

Figure 1

Effect of cortical spreading depression (CSD) on brain activity in normally perfused brain as exemplified in patients with migraine with aura. The figures represent lateral views of the human brain at different intervals after the beginning of the attack, spaced by ∼30 minutes. Outside of attacks, migraine brains have normal perfusion as indicated by the left cartoon. Colored bands indicate region of neuronal depolarization that causes and coincides with depression of cortical activity, a large-scale DC shift, failure of brain ion homeostasis, increased use of O2, glycogen and glucose, and rise in cerebral blood flow (CBF). Light blue area represents reduced CBF, reduced vascular reactivity and neurovascular coupling, and increased CMRO2 in the wake of CSD (Piilgaard and Lauritzen, 2009). The direction of propagation of CSD is indicated with arrows. At the start of migraine attack, a CSD emerges in the occipital pole in patients with a visual aura (1) while spreading anteriorly at the lateral, mesial, and ventral sides of the brain. At the CSD wave front, the transient ionic and metabolic disequilibria trigger the neurological symptoms in eloquent cortex. (2) Following CSD, cortical CBF decreases by 20% to 30%, neurovascular coupling is disturbed, and CMRO2 is increased for >2 hours. (3) Cerebral blood flow in regions not invaded by CSD remains normal. (4) The region of reduced CBF expands as CSD moves anteriorly. (5) Somatosensory symptoms from the extremities appear when the CSD invades the primary sensory cortex at the postcentral gyrus. (6) CSD in patients with migraine usually stops on reaching the central sulcus, but in many patients it does not even propagate this far. In patients with acute brain disorders, the susceptibility of the cerebral cortex to CSD is increased and propagation patterns are more diverse. (7) Full-scale attack. The CSD has stopped and is now detectable as a persistent reduction of cortical blood flow, neurovascular dysfunction and high-energy metabolism. After the attack, the cerebral cortex returns to normal. Modified with permission after original artwork presented in Lauritzen (1987).