Ischemic cerebrovascular events: epidemiology, pathophysiology, clinical, diagnostic interpretation techniques and current affairs

The acute cerebrovascular event is an abrupt episode of neurological dysfunction caused by a vascular stenosis or occlusion that leads to a focal cerebral, spinal, or retinal infarction in a specific vascular territory. In the usual way, the brain uses 20% of cardiac output to maintain the necessary amount of glucose and oxygenation, which is equivalent to a volume of 1 liter of blood or, specifically, a volume per minute of 60 mL / min of perfusion in the gray matter and 25 mL / min in the white matter. To ensure adequate cerebral flow at different pressures and metabolic states, our body regulates blood volume that depends on factors such as oxygen concentration, carbon dioxide and vasodilation or endothelial vasoconstriction. The main regulator of perfusion is exerted by the endothelium, through the effect produced by nitric oxide (NO). When, due to a decrease in cerebral perfusion, the minute volume falls below said threshold, it initiates a process of alteration in cellular functions and changes within the neurovascular unit made up of endoterial cells, surrounding pericytes, basement membrane, perivascular astrocytes, and surrounding neurons. In the process, a cascade of events begins that begins with the loss of the usual neuronal electrical activity, continues with processes of toxicity and apoptosis until reaching the total bioenergetic failure and the death of neural tissue, changes that occur from greater to lesser degree from the area with less blood flow or ischemic nucleus and towards its periphery with less degree of affection as it approaches other vascular territories that can partially supply cerebral perfusion, said intermediate zone between the nucleus of infarction and the brain of other vascular regions is It is known as the penumbra or salvage zone and it is the objective of the treatment to avoid that it is equated with the ischemic nucleus. Among the most common causes of cerebral ischemia are atherosclerosis of the great vessels (15-45%), emboli of cardiac origin (15-30%), small vessel infarcts or lacunar infarcts (15-30%), cryptogenic infarcts (up to 40%) and those of infrequent or unknown cause (less than 5%). The cascade of events that occurs with ischemia leads to cytotoxic edema in the first place. From the point of view of medical images, this change translates in the brain tomography without intravenous contrast in a decrease in the Houndsfiel units (HU) of the infarct site that is evident after 6 hours or after minutes by means of magnetic resonance imaging. nuclear in diffusion sequences (DWI). There are methods of quantification of the infarct zone that depend on the measurement of the volume per minute of a specific segment of the brain, which is defined according to the clinical picture of the most basal or cortical affection. These imaging methods are known as cerebral perfusion and are reproducible in both tomography and magnetic resonance imaging. Angiographic reconstruction by tomography, magnetic resonance or angiography can be used to identify the area of vascular affection, the latter being the ' gold standard 'for the determination of the site of the affection. After determining the area of parenchymal involvement, its infarct nucleus and penumbra or salvage area, as well as the responsible blood vessel, a rapid start of medical or mechanical reperfusion treatments is required, which are indicated according to clinical care algorithms for ensure effective and prompt treatment, avoiding complications associated with it as much as possible. All this should be remembered depends on an early diagnosis of the event, early notification to the emergency services, rapid assessment by neurology and radiology, early use of intravenous thrombolytic therapy and considering the use of mechanical reperfusion techniques in the indicated cases, as well. as units of intensive care of the patient after the initial treatment and rehabilitation. In the following review, the most current known points of clinical and radiological diagnosis will be exposed, as well as the management of cerebral stroke, starting first with a general idea of brain anatomy and then addressing the scales for clinical and radiological diagnosis, by means of the interpretation techniques, their uses both in isolation and as a whole, and the current recommendations for their implementation according to the level of resolution capacity. As far as possible, an attempt will be made to cite national and epidemiological statistics, as well as the management guidelines that it currently has