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Stroke and transient ischemic attack

Transient ischemic attack (TIA) is a sudden, transient and reversible neurological dysfunction caused by focal cerebral ischemia due to transient blood supply deficiency in the carotid or vertebrobasilar artery system. The attack lasts for several minutes, usually completely recovered within 30 minutes, more than 2 hours, often left with mild neurological defects, or CT and MRI showed signs of cerebral ischemia. TIA usually occurs between 34 and 65 years old, accounting for 25.3% over 65 years old. Come on suddenly, come on in the case such as position change, activity overmuch, neck turns suddenly or bend extend. There was no premonition of the disease and transient signs of nervous system localization. General unconsciousness obstacle, last for 5 ~ 20 minutes, can break out repeatedly, but recover completely inside 24 hours commonly, without sequela.

The cause of
The etiology and pathogenesis of transient ischemic attack are still controversial. Most of them are related to the following issues:
Cerebral atherosclerosis
Cerebral atherosclerosis is a part of systemic arteriosclerosis. The grey-yellow plaques on the surface of arterial intima, the continuous proliferation of collagen fibers on the surface of plaques and the proliferation of smooth muscle cells containing lipids cause arterial stenosis. Even the deep layer of the fiber plaque cells necrosis, the formation of atheromatous plaque, atheromatous plaque surface of the fiber cap necrosis, ulceration formation. Necrotic atheromatous plaque material can be discharged into the blood and cause embolism, bleeding ulcer can form hematoma, make small artery lumen stenosis or even obstruction, make blood supply obstacles. The etiology of atherosclerosis mainly includes: hypertension, hyperlipidemia, diabetes, smoking, obesity, insulin resistance and other factors. Most scholars believe that the pathogenesis of atherosclerosis is a complex and comprehensive long process.
2. Micro embolism
Aorta and the contents of cerebral atherosclerotic plaque and its mural thrombus in the ulcer occurred clot, can become small emboli in the blood, scattered, cholesterol crystals by cellulose, platelets, white blood cells of small emboli, circulating blood flow into the small arteries, which can cause microemboli, cause ischemia symptoms. The microembolus is decomposed by the action of enzyme, or the distal end of the embolism is ischemic and dilated, so that the embolus moves to the blood ending, the blood supply is restored, and the symptoms disappear.
Heart disease
Heart disease is the third risk factor for cerebrovascular disease. All kinds of heart disease such as rheumatic heart disease, coronary atherosclerosis, heart disease, hypertensive heart disease, congenital heart disease, and may concurrently various cardiac damage such as atrial fibrillation, atrioventricular block, cardiac insufficiency, left heart hypertrophy, bacterial endocarditis, etc., these factors of hemodynamic effects and embolic loss increases the risk of cerebrovascular disease, especially the risk of ischemic cerebrovascular disease.
4. Hemodynamic changes
Rapid head rotation or neck flexion and extension can alter cerebral blood flow and lead to dizziness. Severe cases can trigger transient ischemic attacks. In particular, atherosclerosis, cervical spondylosis, foramen magnum malformation, carotid sinus allergy and other conditions are more likely to occur. The pathological changes of aortic arch and subclavian artery can cause blood stealing syndrome and affect the blood supply to the brain.
Changes in blood composition
Transient ischemic attack can be triggered by changes in blood composition and blood pathological status that affect blood oxygen, blood sugar, blood lipids, blood protein content, blood viscosity and coagulability, such as severe anemia, polycythemia, leukemia, thrombocythemia, abnormal proteinemia, and high lipoprotein plasma.

Clinical manifestations of
1. Transient ischemic attack of internal carotid artery system
The most common symptoms of internal carotid artery TIA are hemiplegia, hemiplegia, hemiparesis, aphasia, monocular visual impairment, etc.
Main performance: monocular sudden appearance of transient amaurosis, or vision loss, or white flashing, or visual field defect, or double vision, lasting several minutes can be recovered. Mild hemiparesis or hemiparesthesia of the contralateral limb. Transient aphasia or aphasia, or loss of reading or writing, or simultaneous facial and lingual muscle weakness occurred in the dominant hemisphere. I occasionally have ipsilateral hemianopia. Sudden transient amaurosis of one eye is a characteristic symptom of ischemia of the internal carotid artery. Transient psychiatric symptoms and disturbance of consciousness are occasionally seen.
2. Vertebrobasilar artery system transient ischemic attack
Vertebrobasilar artery TIA is mainly manifested as cerebral stem, cerebellum, occipital lobe, temporal lobe and proximal spinal cord ischemia, nerve defects.
The main symptoms are: the most common symptoms are transient dizziness, nystagmus, and instability in standing or walking. Transitory binocular vision or visual field defect, etc. Transient dysphagia, choking on drinking water, slurred speech or hoarseness. Transient unilateral or bilateral limb weakness, paresthesia. Transient hearing loss, intersectional paralysis, hemiplegia and bilateral mild paralysis. A few may have conscious disturbance or cataplexy.



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