What Is a Brain Attack?

Transient ischemic attack (TIA) is a transient insufficient blood supply to the carotid artery or vertebral-basal artery system, causing focal cerebral ischemia leading to sudden, transient, and reversible neurological dysfunction. Seizures last for several minutes, and usually fully recover within 30 minutes. Minor neurological deficits are often left over 2 hours, or CT and MRI show signs of cerebral ischemia. TIA occurs in 34 to 65 years old, 25.3% of them are over 65 years old, and more men than women. Sudden onset of the disease, mostly in the body position changes, excessive movement, sudden neck rotation or flexion and extension, etc. There is no threat of onset, and there are transient signs of localization of the nervous system. Generally unconscious disorder, which lasts 5 to 20 minutes, can be recurrent, but generally fully recovered within 24 hours, no sequelae.

Basic Information

Visiting department: Neurology
Multiple groups: 34 to 65 years old male
Common causes: Cerebral atherosclerosis, microembolism, heart disease, changes in hemorheology, changes in blood components, etc.

Common symptoms: Monoplegia, Hemiplegia, Hemiplegia, Aphasia, Monocular Vision Impairment, Isotropic Blindness, Transient Dizziness, Eye Shock, Standing or Walking Instability

Causes of Transient Ischemic Attack

There are still differences and debates about the etiology and pathogenesis of transient ischemic attacks. Most consider it related to the following issues:

Cerebral atherosclerosis

Cerebral atherosclerosis is part of systemic arteriosclerosis. The gray-yellow plaques on the surface of the intima of the arteries, the collagen fibers on the surface of the plaques continue to proliferate and the smooth muscle cells containing lipids cause arterial stenosis. Even the cells deep in the fibrous plaques became necrotic, forming atherosclerotic plaques, and the fibrous caps on the surface of the atherosclerotic plaques were necrotic and ulcerated to form ulcers. Necrotic atheromatous plaque material can be discharged into the blood and cause embolism. The ulcers can bleed to form hematomas, narrow the arterial lumen, and even block the blood supply. The main causes of atherosclerosis include: hypertension, hyperlipidemia, diabetes, smoking, obesity, insulin resistance and other factors. Most scholars believe that the pathogenesis of atherosclerosis is complex and a comprehensive long process.

2. Microembolism

The contents of the aortic and cerebral atherosclerotic plaques and the debris of the mural thrombus clots when they ulcerate can be scattered in the blood stream to become microemboli. This type of cellulose, platelets, white blood cells, cholesterol Microemboli composed of crystals, circulating blood flow into the arterioles, can cause microemboli, causing ischemic symptoms. The microemboli are broken down by the action of enzymes, or due to the ischemic dilation of the distal blood vessels of the embolism, causing the emboli to move to the blood end, the blood supply is restored and the symptoms disappear.

3. Heart disease

Heart disease is the third risk factor for cerebrovascular disease. Various heart diseases such as rheumatic heart disease, coronary atherosclerotic heart disease, hypertension heart disease, congenital heart disease, and various possible heart damage such as atrial fibrillation, atrioventricular block, heart Insufficiency, left heart hypertrophy, bacterial endocarditis, etc., these factors increase the risk of cerebrovascular disease, especially the risk of ischemic cerebrovascular disease, by affecting hemodynamics and emboli shedding.

4. Hemodynamic changes

Rapid head rotation or neck flexion and extension can change cerebral blood flow and cause dizziness, and severely can trigger a transient ischemic attack. In particular, atherosclerosis, cervical spondylosis, occipital foramen deformities, carotid sinus allergies and other conditions are more likely to occur. Lesions of the aortic arch and subclavian artery can cause blood stealing syndrome and affect the blood supply to the brain.

5. Changes in blood composition

Various changes in blood components and blood pathological conditions that affect blood oxygen, blood glucose, blood lipids, blood protein content, as well as blood viscosity and coagulability, such as severe anemia, erythrocytosis, leukemia, thrombocytosis, abnormal proteinemia, high fat Proteinemia can trigger a transient ischemic attack.

Clinical manifestations of transient ischemic attack

1. Transient ischemic attack of internal carotid artery system

The most common symptoms of TIA in the internal carotid artery system are monoplegia, hemiplegia, hemiplegia, aphasia, and monocular vision impairment. Isotropic hemianopia can also occur.

Main manifestations: transient transient blackness in one eye, or loss of vision, or white flicker, visual field defect, or double vision, which can be recovered for several minutes. Contralateral limbs have mild hemiplegia or paresthesia. The dominant hemisphere is damaged and there is transient aphasia or aphasia or aphasia or aphasia, or weakness of the facial and tongue muscles. Occasional hemianopia. Among them, the sudden appearance of transient blackness in one eye is a characteristic symptom of ischemia of the branch of the internal carotid artery. Transient psychiatric symptoms and disturbances of consciousness are also visible.

2. Transient ischemic attack of vertebral-basal artery system

Vertebro-basal artery system TIA mainly manifests as brain stem, cerebellum, occipital lobe, temporal lobe, and proximal spinal cord ischemia, neurological defects.

The main symptoms are: the most common symptoms are transient dizziness, nystagmus, standing or walking instability. Transient visual objects are doubled or visual field defects. Transient difficulty swallowing, coughing from drinking water, slurred speech, or hoarseness. Transient weakness in one or both limbs and paresthesia. Transient hearing loss, cross paralysis, hemiplegia, and bilateral mild paralysis. A few may have conscious disturbance or sudden onset.

Transient ischemic attack

Hemorheology test

Mainly manifested in the increase of whole blood viscosity, plasma viscosity, hematocrit, fibrinogen and platelet aggregation rate.

2. Cerebrovascular examination

Such as transcranial Doppler examination, carotid B-ultrasound examination, digital subtraction angiography examination, MRA examination and so on.

3. Cervical Spine Examination

X-ray, cervical CT scan or cervical MRI can be used.

4. Head CT scan or MRI

Observe intracranial ischemia and exclude bleeding disorders.

5. ECG

The diagnosis is mainly excluded. Whether the patient has atrial fibrillation, frequent premature beats, old myocardial infarction, left ventricular hypertrophy, etc. Echocardiography checks for the presence of heart valve disease, such as rheumatic valvular disease and senile valvular disease.

Diagnosis of transient ischemic attack

The diagnosis of transient ischemic attack is mainly based on a detailed history, that is, sudden, repetitive, transient, and stereotyped characteristics, combined with necessary auxiliary examinations to diagnose, and other cerebrovascular diseases must be excluded before diagnosis.

Transient ischemic attack treatment

Different treatment methods are adopted according to the form and cause of TIA. Occasionally or only once. In the case of low blood pressure, you can take small doses of enteric-coated aspirin, or clopidogrel for a long time. The application time of aspirin depends on the specific situation of the patient. In most cases, it should be applied for 2 to 5 years. If there are no obvious side effects, the use time can be extended. If there are risk factors causing TIA, the aspirin should be taken for a longer time. At the same time, drugs that prevent vasospasm, such as nimodipine, can also be taken with inositol nicotinate.

Frequent attacks, that is, repeated attacks in a short period of time, should be regarded as a neurological emergency. If patients with frequent TIA attacks are not effectively controlled, and there is a high possibility of cerebral infarction in the near future, they should be actively treated. The principle of treatment is comprehensive treatment and individualized treatment:

1. Actively treat risk factors

Such as hypertension, hyperlipidemia, heart disease, diabetes, cerebral arteriosclerosis and so on.

2. Anti-platelet aggregation

You can choose enteric-coated aspirin or clobidogrel.

3. Improve brain microcirculation

Such as nimodipine, cinnarizine (brainizine) and so on.

4. Vasodilator drugs

For example, Qukerutin (Wei Nao Lu Tong) can be used.

Prognosis of transient ischemic attack

TIA is a chronic recurrent clinical syndrome. During the onset of TIA, obvious localized brain dysfunction may appear. This affects patients' quality of life and work ability, and weakens the patient's ability to adapt to society to varying degrees.

It is generally believed that the incidence of cerebral infarction after TIA is 4% to 8% in the first month, 12% to 13% in the first year, 24.29% after 5 years, and the annual incidence of cerebrovascular disease in the first 5 years It was 5.9%. After suffering from TIA, patients are extremely worried about the prognosis of the disease, which leads to emotional disorders such as anxiety, doubt, and depression. Negative emotions can affect the neuroendocrine system and aggravate changes in mental state.

In addition, the prognosis of TIA is related to frail elderly, high blood pressure, diabetes, heart disease, etc. If the onset of TIA is not controlled in time, it may eventually lead to cerebrovascular disease. If the TIA is treated in time, the prognosis is good.