Brief introduction of cerebral infarction
Cerebral infarction is an atherosclerotic cerebral infarction, which refers to atherosclerosis and thrombosis in the arterial system of the brain (mainly internal carotid artery-middle cerebral artery system or vertebral-basilar artery system), which narrows and blocks the arterial lumen and leads to local brain tissue necrosis in the arterial blood supply area. Clinical manifestations are hemiplegia, hemiplegia, slurred speech and other sudden symptoms of local neurological deficit, formerly known as cerebral thrombosis. This disease is the most common cerebrovascular disease, accounting for 70% of cerebrovascular diseases. The incidence rate of elderly people over 55 years old is high, which is higher in men than in women.
Clinical manifestations: 1. The onset is sudden, usually starting from one upper limb, and then the symptoms of neurological dysfunction gradually affect other parts of the other limb within a few hours or a day or two.
2. Most of them are not accompanied by symptoms of increased intracranial pressure, such as headache and vomiting. Secondary brain edema occurring within a few days after occlusion of the aorta can worsen symptoms and lead to disturbance of consciousness. Severe brain edema can also lead to fatal brain hernia.
3. Middle cerebral artery and its deep perforating branches: the most easily involved, including contralateral hemiplegia (severity), unilateral numbness (loss of sensation) and ipsilateral hemianopia. When the main hemisphere (usually the left side) is involved, it can show aphasia, and when the non-dominant hemisphere is involved, it will produce apraxia.
4. Internal carotid artery: it can cause ipsilateral blindness, and other symptoms are often indistinguishable from the symptoms and signs after occlusion of the middle cerebral artery and its deep perforating branches.
5. Anterior cerebral artery: rare, one side can cause contralateral hemiplegia (heavy lower limbs and light upper limbs), strong grip reflex and urinary incontinence. Bilateral involvement can cause apathy and confusion, and occasionally silence and spastic paraplegia.
6. Posterior cerebral artery: unilateral hemianopia, disappearance of contralateral hemiplegia, spontaneous thalamic pain, or sudden involuntary hemiplegia; When the dominant hemisphere is involved, alexia can be seen.
7. Vertebrobasilar artery: eye movement paralysis, abnormal pupil, quadriplegia, difficulty in eating and swallowing, disturbance of consciousness and even death.
The diagnosis is based on 1. The onset age is mostly over 50 years old, with a history of hypertension and diabetes or signs of atherosclerosis;
2. Cerebral artery occlusion syndrome such as contralateral hemiplegia (severity), unilateral numbness (loss of sensation), homonymous hemianopia, aphasia, apraxia, dizziness, diplopia, eye movement paralysis, ataxia, cross paralysis, abnormal pupil, quadriplegia, difficulty in eating and swallowing, and disturbance of consciousness.
3. Brain CT examination is negative or the low density of brain tissue conforms to the distribution of blood vessels, or brain magnetic resonance imaging shows that the source of ischemia or edema conforms to the distribution of blood vessels.
4 treatment principles 1. Treatment of primary diseases such as hypertension, diabetes and atherosclerosis.
2. Anticoagulation therapy.
3. Vasodilators.
4. Reduce blood lipid and blood viscosity
5. Vascular surgery, intima and plaque removal or angioplasty.
6. Symptomatic treatment and treatment of complications.
5 medication principle 1. Hypertension and arteriosclerosis should be treated in time;
2. Intravenous infusion of anticoagulants such as heparin or newly reported low molecular weight heparin can stabilize progressive stroke, but it is ineffective for acute complete stroke. The bleeding side effects caused by anticoagulants (especially heparin) in hypertensive patients should be banned.
3. For those who have not used anticoagulants, aspirin, dipyridamole and other drugs can be used. Selebidine (Likang suppository) is a more effective new specific drug.
4. Low molecular dextran helps to reduce blood viscosity; Vasodilators (nifedipine, nicotinic acid, etc. ) and traditional Chinese medicine should be used with caution according to specific patients.
6. Auxiliary examination 1. Pay attention to determine whether there are diseases such as hypertension, severe anemia, polycythemia and infection during physical examination; Detailed nervous system examination is helpful to locate occluded blood vessels;
2. CT examination of the brain to diagnose and accurately judge the location and scope of infarction; Patients with onset within 2448 hours and normal CT examination can choose brain magnetic resonance imaging, which can show the location and scope of cerebral infarction and brain edema earlier and more accurately, which is helpful to diagnose the cause of cerebral infarction.
3. The cerebral vessels were examined by Doppler ultrasound to detect the blood flow of different cerebral vessels and the changes of local vascular wall. Magnetic resonance angiography (MRA) and digital subtraction angiography (DSA) are helpful for the etiological diagnosis of patients with unknown causes.
4. Routine and liver and kidney function tests to understand the functions of other organs of patients;
5. Blood lipid, blood sugar and hematology examination for etiological diagnosis.
7 efficacy evaluation 1. Cure: clear consciousness, stable blood pressure, good recovery of limb movement, feeling and language function, self-care in life, and signs of mild nerve injury.
2. Improvement: the consciousness is clear, and the physical and language functions have been improved to varying degrees.