Cortical spreading depolarization: Pathophysiology, implications, and future directions.

摘要: Cortical spreading depolarization (CSD) is a loss of ion homeostasis, altered vascular response, change in synaptic architecture, and subsequent depression electrical activity following an inciting neurological injury. First described by Leao 1944, this disturbance neuronal electrophysiology has since been demonstrated number animal studies, recently few human studies that examine the occurrence depolarizing phenomenon setting variety pathological states, including migraines, cerebrovascular accidents, epilepsy, intracranial hemorrhages, traumatic brain injuries. The onset CSD experimentally disruption environment leading to glutamate-induced toxicity. This initial event leads changes channels maintain membrane potential. Recovery mechanisms such as sodium-potassium pumps aim restore homeostasis fail, osmolar shifts fluid, swelling neuron, ultimately measurable cortical spreads order millimeters per minute. Equally important resulting response. In healthy tissue, increased coupled with release vasodilatory factors nitric oxide arachidonic acid metabolites increase local blood flow meet energy expenditure. damaged not only restorative response lacking but vasoconstrictive promoted ischemia follows adds severity Tissue threatened ischemic then at elevated risk for propagation falls into vicious cycle hemodynamic disturbance. Efforts have made halt using N-methyl-D-aspartate receptor antagonists other channel blockers minimize damaging effects can persist long after triggering insult.