Evidence for CSD or CSD-Like Phenomena in Human Brain in Relation to Migraine and Stroke

Abstract

Cortical spreading depression (CSD) is associated with a dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, and increased energy metabolism. There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine. Based on the experience related to the detection of CSD in humans, we discuss pitfalls and possible strategies for detecting CSD in humans. In the border zone of an infarct, cells are capable of surviving if protected from the dramatic failure of brain ion homeostasis that is a consequence of the shortage of substrate supply in that region. The ion failure can be monitored by transient depolarization shifts. The recurrent transient perturbations in the border zone of an infarct (now often designated periinfract depolarisations, or PIDs) are reminiscent of CSD. The development of reliable methods for detecting CSDs or PIDs in humans will determine the extent to which the large body of experimental findings from animal studies of CSD can be applied to the investigation and treatment of human brain disease.