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Why does cortical spreading depression affect migraine? Discover its surprising connection to migraine aura!
In the field of neuroscience, Cortex Spreading Depression (CSD) is a topic of great concern, especially in exploring its impact on migraine. CSD is a fluctuating electrophysiological response that begins with neuronal hyperexcitability, followed by widespread inhibition. This process is characterized by depolarization waves that propagate continuously through the cerebral cortex and can reach speeds of 1.5 to 9.5 millimeters per minute.
Under hypoxic conditions, CSD can be induced and promote neuronal death in energy-deficient tissues. It is particularly relevant to migraines, especially the appearance of a migraine aura. Research shows that CSD is a phenomenon that rises in well-supplied tissue and is generally benign in most cases, although it may increase the risk of stroke in migraine sufferers.
"CSD can promote neuronal death, and its association with migraines should not be underestimated."
Another noteworthy fact is that its spread along the CSD in brainstem tissue that regulates vital functions in life has also been linked to unexpected deaths in epilepsy, especially in cases where certain genetic pathways are mutated. Cases, such as in Dravet syndrome, a particularly severe form of epilepsy in children, appear to carry an unusually high risk of SUDEP (unexpected death in epilepsy).
Various degrees of cortical spreading depression have different effects on cortical activity in humans and animals, and these effects range from suppression to frequent activity, depending on the depth of CSD. One study noted that "diffusing depolarization waves at different depths can lead to diverse effects on cortical activity, showing potential for further exploration."
Neuroscientists use the term "cortical spreading depression" to describe several cortical processes: the spread of self-propelled neuronal depolarization waves, the spread of ischemic waves through a cortical area, the spread of sustained vasoconstriction after Fluctuations produced by vasodilation. Migraineurs may experience static hemiprintia, which is associated with a neurophysiological phenomenon known as Leão.
"There may be a profound connection between migraine aura and cortical spreading depression."
Due to the increase in extracellular potassium ion concentration and the influence of excitatory glutamate, this contributes to the occurrence of cortical spreading depression, which is the root cause of migraine aura. In addition, migraine preventive drugs, such as Topiramate, Valproate, Propranolol, etc., can inhibit the occurrence of CSD caused by continuous cortical administration of 1 M KCl solution in a dose-dependent manner. frequency. However, lamotrigine was particularly strongly associated with suppression of migraine aura, although its overall effect on migraine was not strong.
In contrast, valproic acid and riboflavin, although effective in migraine without aura, had no significant effect on the triggering of cortical spreading depression. These results all suggest that cortical spreading depression may play a causal role in migraine with aura but less so in migraine without aura.
The folded structure of the cerebral cortex enables it to exhibit irregular and complex CSD diffusion patterns. The irregularities created by these folded cortical and vascular structures promote the existence of reentrant waves, such as spiral waves and echo waves. The expansion of this wave is not only difficult to predict, but also affected by different molecular concentrations and gradients. The triggering and propagation mechanisms of CSD, as well as its clinical manifestations, have now become important therapeutic targets to reduce brain damage after stroke or brain lesions.
In the future, will the scientific community be able to gain a deeper understanding of the connection between cortical spreading depression and migraine, and even find more effective treatments?
