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Cerebral infarction, also known as an ischemic stroke, is the pathologic process that results in an area of necrotic tissue in the brain (cerebral infarct). [1] In mid to high income countries, a stroke is the main reason for disability among people and the 2nd cause of death. [2]
The underlying mechanism involves the nervous system slowing the heart rate and dilating blood vessels, resulting in low blood pressure and thus not enough blood flow to the brain. [2] Diagnosis is based on the symptoms after ruling out other possible causes. [3] Recovery from a reflex syncope episode happens without specific treatment. [2]
Similar failure processes are involved in brain failure following reversal of cardiac arrest; [3] control of these processes is the subject of ongoing research. Repeated bouts of ischemia and reperfusion injury also are thought to be a factor leading to the formation and failure to heal of chronic wounds such as pressure sores and diabetic foot ...
Brain ischemia has been linked to a variety of diseases or abnormalities. Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison to the average population.
The periaqueductal gray (PAG), also known as the central gray, is a brain region that plays a critical role in autonomic function, motivated behavior and behavioural responses to threatening stimuli. [1] [2] PAG is also the primary control center for descending pain modulation. It has enkephalin-producing cells that suppress pain.
Watershed stroke symptoms are due to the reduced blood flow to all parts of the body, specifically the brain, thus leading to brain damage. Initial symptoms, as promoted by the American Stroke Association, are FAST, representing F = Facial weakness (droop), A = Arm weakness (drift), S = Speech difficulty (slur), and T = Time to act (priority of intervention).
The locus coeruleus is the major source of noradrenergic innervation in the brain and sends widespread connections to rostral (cerebral cortex, hippocampus, hypothalamus) and caudal (cerebellum, brainstem nuclei) brain areas [24] and. [25] Indeed, an alteration of this structure could contribute to several symptoms observed in MECP2-deficient mice.
This decrement or suppression of the P1 represents the cost of having to stop attending to one area and shift the attention to the place where the target stimulus is located. This is as compared to another component called the N1.