Migrainous Infarction and Cortical Spreading Depression. Discoveries (Craiova, Romania) Migraine is a very common disorder of the nervous system. It shares similar physiological processes with stroke. Migrainous infarction is a rare complication of migraine with aura. The neuro-logical symptoms of migraine aura correspond to the cortical spreading depression and this depression can lead to a migrainous infarction. It is pertinent to state that the investigation and detection of the cortical depression might have a great clinical significance. Blood vessels in the cranium play an important role in the pathophysiology of migraine.  In the case of injured states of brain, the cortical spreading depression causes extreme vasoconstriction rather than vasodilation. The endothelial damage caused by the cortical spreading depression can result in hypercoagulability, leading to an increased risk of stroke. There are many genetic disorders in which migraine and stroke are the major symptoms and an insight into these disorders can help us in the understanding of complex mechanisms of migrainous infarction. It is pertinent to state that some derangements in the vascular function accompany migraine which may also serve as targets for research and treatment. This article will describe the hemodynamic and genetic relationship between migraine induced stroke and how it relates to the cortical spreading depression. 10.15190/d.2020.9

Cortical Spreading Depression and Ischemia in Neurocritical Patients. Wainsztein Néstor,Rodríguez Lucci Federico Neurosurgery clinics of North America Spreading depolarization in cerebral cortex is associated with swelling of neurons, distortion of dendritic spines, massive ion translocation with a large change of the slow electrical potential, and silencing of brain electrical activity. The term spreading depression represents a wave of spontaneous activity of the electrocorticogram that propagates through contiguous cerebral gray matter at a characteristic velocity. Spreading depression is a consequence of cortical spreading depolarization. Therefore, spreading depolarization is not always accompanied by spreading depression and the terms are not synonymous. 10.1016/j.nec.2017.11.003

Dynamics of Ionic Shifts in Cortical Spreading Depression. Cerebral cortex (New York, N.Y. : 1991) Cortical spreading depression is a slowly propagating wave of near-complete depolarization of brain cells followed by temporary suppression of neuronal activity. Accumulating evidence indicates that cortical spreading depression underlies the migraine aura and that similar waves promote tissue damage in stroke, trauma, and hemorrhage. Cortical spreading depression is characterized by neuronal swelling, profound elevation of extracellular potassium and glutamate, multiphasic blood flow changes, and drop in tissue oxygen tension. The slow speed of the cortical spreading depression wave implies that it is mediated by diffusion of a chemical substance, yet the identity of this substance and the pathway it follows are unknown. Intercellular spread between gap junction-coupled neurons or glial cells and interstitial diffusion of K(+) or glutamate have been proposed. Here we use extracellular direct current potential recordings, K(+)-sensitive microelectrodes, and 2-photon imaging with ultrasensitive Ca(2+) and glutamate fluorescent probes to elucidate the spatiotemporal dynamics of ionic shifts associated with the propagation of cortical spreading depression in the visual cortex of adult living mice. Our data argue against intercellular spread of Ca(2+) carrying the cortical spreading depression wavefront and are in favor of interstitial K(+) diffusion, rather than glutamate diffusion, as the leading event in cortical spreading depression. 10.1093/cercor/bhv054