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How does the brain become a 'lightning storm'? Learn more about the mysterious process of cortical spreading depression!
In the secret world of how the brain works, there is a fascinating yet mysterious phenomenon called cortical spreading depression (CSD), or spreading depolarization (SD). This is a fluctuation dominated by electrophysiological activity. After experiencing a violent fluctuation for more than one second, an inhibitory wave follows. However, this process is not only a "lightning storm" in the brain, but also reveals some potential health problems.
The phenomenon of diffuse depolarization is dominated by depolarization waves in neurons and glia that propagate across the cortex at velocities of 1.5 to 9.5 millimeters per minute.
Cortical spreading depression can be triggered by hypoxia and promotes neuronal cell death in energy-deficient tissues, a phenomenon closely associated with migraine auras. While in most cases this spreading wave is benign, in some migraine sufferers it may increase the chance of stroke. Research in recent years has shown that the onset of this spreading depression, especially in brainstem tissues that control survival functions, may be related to sudden unexpected death (SUDEP) in patients with epilepsy.
The association between CSD and nerve potential abnormalities makes it a research focus for prevention and treatment in patients with epilepsy and migraine.
Although the terms "cortical spreading depression" and "diffusing depolarization" are often used interchangeably, research has found that spreading depolarization can have diverse effects on cortical activity in humans and mice, ranging from suppression to peak activity. The changes depend on the depth of depolarization. This allowed scientists to realize that the complexity of cortical structures does affect the propagation pattern of CSD.
Multiple aspects of cortical spreading depression
Neuroscientists use the term "cortical spreading depression" to describe several cortical processes: the spread of self-propagating waves of cellular depolarization through the cerebral cortex; ischemic surges through specific regions; and the persistence of vasodilatation that occurs after vasodilation. Sexual vasoconstriction wave, etc. These phenomena are invariably linked to the pathogenesis of migraine.
Increased extracellular potassium concentrations and excitatory glutamate contribute to the initiation and extension of cortical spreading depression.
Studies have found that some migraine preventive drugs that are used repeatedly and daily, such as topiramate, valproic acid, propranolol, etc., can inhibit CSD in a dose-dependent manner, while some drugs, such as lamotrigine, focus on migraine. Specific inhibitory effects of headache aura. These findings highlight the causal role of CSD in migraine patients with auras, whereas in migraine patients without auras, the same factor does not play a role.
Complex transmission patterns and clinical significance
The complex folding structure of the cerebral cortex creates irregular and complex CSD propagation patterns. This diversity arises not only from the morphology of the brain but also from the structure of blood vessels, optimizing the presence of reentrant waves such as spirals and echoes. As the wave expands, its course becomes more unpredictable and affected by different molecules and concentration gradients.
In-depth research on the triggering and propagation mechanisms of CSD and its clinical manifestations may become therapeutic targets to reduce brain damage after stroke or brain injury.
In the process of exploring cortical spreading depression, we cannot help but ask, does this phenomenon, which changes as fast as lightning in the brain, reveal a more profound truth about the operation of human thinking?
