Cerebral infarction

Introduction to brain infarction Cerebral infarction (Cerebralinfarction, CI) is a general term for ischemic stroke, including cerebral thrombosis, lacunar infarction and cerebral embolism, accounting for about 70% of all strokes. It is a brain blood supply disorder causing brain lesions. . Cerebral infarction is caused by the sudden decrease or stop of blood flow in the local blood supply artery of the brain tissue, resulting in ischemia and hypoxia of the brain tissue in the blood supply area of the blood vessel, leading to necrosis and softening of the brain tissue, accompanied by clinical symptoms and signs of the corresponding parts, such as hemiplegia. Symptoms such as aphasia and neurological deficits. After 24 to 48 hours of onset of cerebral infarction, brain CT scans show low-density lesions at corresponding sites. The boundary is not clear and may have a certain occupancy effect. Brain MRI can detect cerebral infarction at an early stage. It shows that T1 has a low signal in the lesion area, T2 shows a high signal, and MRI can find a small infarct. Many people in the clinic have no cerebrovascular disease even if they have the risk factors of cerebrovascular disease mentioned above, while others who do not have the risk factors of cerebrovascular disease have cerebrovascular disease, indicating that the occurrence of cerebrovascular disease is related to other factors. Especially related to genetic factors. The family history of cerebrovascular disease may be a risk factor for cerebrovascular disease. Some people have also shown that there is hypertension, the incidence of diabetes and the family history of cerebrovascular disease. The number of cases is significantly higher than that of the control group. The incidence of cerebrovascular disease is multifactorial, and it is the result of the combination of genetic and environmental factors. For example, the incidence of cerebrovascular disease has a certain ethnic difference, and the incidence of black blood cerebrovascular disease is higher than that of Caucasian. basic knowledge Sickness ratio: 0.1% Susceptible people: people over 50 to 60 years old Mode of infection: non-infectious Complications: hemorrhoids, sudden death, cerebral palsy

Cause of brain infarction

Causes:

Lesions of the vessel wall itself (25%):

The most common is atherosclerosis, which is often associated with risk factors such as hypertension, diabetes, and hyperlipidemia. It can lead to cerebral artery stenosis or occlusive disease, but the arterial involvement of large and medium-sized tube diameter (500m) is more common. The intracranial artery disease of Chinese people is more common than that of extracranial artery disease. Followed by inflammation of the cerebral artery wall, such as tuberculosis, syphilis, connective tissue disease. In addition, congenital vascular malformations, vascular wall dysplasia, etc. can also cause cerebral infarction. Because atherosclerosis occurs in the bifurcations and bends of large blood vessels, the most common sites of cerebral thrombosis are the beginning and siphon of the carotid artery, the beginning of the middle cerebral artery, the vertebral artery and the basilar artery. The next paragraph and so on. When plaques on the intima of these sites rupture, forms of blood in platelets and cellulose form adhesion, aggregation, and deposition to form a thrombus, and thrombus detachment forms an embolus that blocks the distal artery and causes cerebral infarction. Cerebral arterial plaque can also cause significant stenosis or occlusion of the lumen itself, causing blood pressure drop, slowing of blood flow velocity and increased blood viscosity in the perfusion area, resulting in a decrease in blood supply to the local brain region or promotion of local thrombosis. symptom. [1]

Blood composition changes (22%):

Thrombosis can be caused by polycythemia vera, hyperviscosity, hyperfibrinogenemia, thrombocytopenia, oral contraceptives, and the like. In a few cases, there may be high levels of antiphospholipid antibodies, protein C, protein S or hypercoagulable state associated with antithrombotic III deficiency. These factors can also cause embolic events in the cerebral arteries or in situ cerebral arterial thrombosis.

Bad living habits (25%):

1 smoking, alcoholism: the number of smokers in patients with cerebrovascular disease is significantly higher than that of patients with non-cerebral vascular disease, and smoking is positively correlated with the occurrence of cerebrovascular disease. Alcohol abuse is definitely a bad habit. Alcoholism is a significant hypertension. Risk factors, and hypertension is the most important risk factor for cerebrovascular disease.

2 constipation: Chinese medicine believes that the incidence of cerebrovascular disease has a certain regularity, which may be related to constipation. It should help to reduce the possibility of cerebrovascular disease through dietary adjustment and regular bowel habits.

3 physical exercise, overweight and cerebrovascular disease: the proportion of people who usually exercise in cerebrovascular disease is significantly lower than that of non-cerebral vascular disease control group, and the number of overweight cerebrovascular disease is significantly higher than that of non-cerebral vascular disease control group. Balanced diet, weight control and physical exercise can reduce the incidence of cerebrovascular disease.

4 high-salt diet: high-salt diet is generally considered to be a risk factor for hypertension. Hypertension is the most important risk factor for cerebrovascular disease. Therefore, low-salt diet is recommended. The diet can increase the intake of vinegar to facilitate calcium. absorb.

Family history of genetics (10%):

Many people in the clinic have no cerebrovascular disease even if they have the risk factors of cerebrovascular disease mentioned above, while others who do not have the risk factors of cerebrovascular disease have cerebrovascular disease, indicating that the occurrence of cerebrovascular disease is related to other factors. Especially related to genetic factors. The family history of cerebrovascular disease may be a risk factor for cerebrovascular disease. Some people have also shown that there is hypertension, the incidence of diabetes and the family history of cerebrovascular disease. The number of cases is significantly higher than that of the control group. The incidence of cerebrovascular disease is multifactorial, and it is the result of the combination of genetic and environmental factors. For example, the incidence of cerebrovascular disease has a certain ethnic difference, and the incidence of black blood cerebrovascular disease is higher than that of Caucasian.

Pathological changes:

(1) The central area of acute cerebral infarction is necrotic brain tissue, surrounded by edema area, cerebral edema in the early stage of infarction, edema is also obvious in infarct area, and the infarct size is relatively small, edema area is relatively small, edema The cerebral gyrus is flattened and the sulci disappears. When the infarct size is large and the whole hemisphere is edematous, the midline structure is displaced. In severe cases, cerebral palsy may be formed, and the diseased tissue is atrophied in the later stage. The necrotic tissue is cleared by the lattice cells, leaving empty The scar tissue of the cavity, the old thrombus can be seen in the internalization and lumen recanalization, the arteriosclerotic cerebral infarction is generally white infarction, and the necrotic vessels in a few infarct areas can be secondary to rupture and cause bleeding, called hemorrhagic infarction or red infarction. .

(2) Disease physiological changes:

1 The content of vasoactive substances changes: the content of tumor necrosis factor in cerebral infarction is significantly increased, in addition, NO, endothelin, calcitonin gene-related peptide, neuropeptide Y are also increased, neuropeptide Y and neurotensin are The neuroendocrine polypeptide of the cardiovascular and cerebrovascular system plays an important regulatory role. During the pathogenesis of acute cerebrovascular disease, tumor necrosis factor, nitric oxide, endothelin, neuropeptide Y, calcitonin gene-related peptide and neurotensin change, This change is closely related to the nature of the disease and the condition of acute cerebrovascular disease. Active control of the balance disorder between these substances will help to reduce the mortality and morbidity rate of acute cerebrovascular disease.

2 Hypothalamic-pituitary hormone release: The two systems of nerve and endocrine have their own characteristics and are closely related, and jointly regulate and integrate the balance of internal and external environment, and the release of hypothalamic-pituitary hormone in patients with cerebrovascular disease is enhanced. It may directly invade tissues such as the hypothalamus, pituitary gland, or the vascular dysfunction caused by cerebral edema.

3 changes in plasma coagulation factors: increased factor VII (FVII) activity is a risk factor for ischemic cerebrovascular disease, or even associated with myocardial infarction and sudden death.

4 Nitric oxide changes: the role of nitric oxide (NO) is related to the time of its production, tissue source and content, and tissue nitric oxide synthase (cNOS) on endothelial cells, which relies on calcium in the early stage of cerebral infarction. / Calmodulin (Ca2 / CaM) activation, causing short-term release of NO, causing blood vessels to dilate, producing a beneficial effect, in addition, in macrophages, inducible NOS (iNOS) on glial cells, it does not depend on Ca2 / CaM is not activated under physiological conditions. After 1 to 2 days after cerebral infarction, iNOS is activated. Once activated, NO is continuously produced. Continuous NO production can cause cytotoxicity, so iNOS is activated in the acute phase of cerebral infarction. May aggravate ischemic damage.

5 hypothalamic-pituitary-gonadal axis changes: acute cerebrovascular disease can lead to functional changes in the hypothalamic-pituitary-gonadal axis, and different sexes, different disease types, the changes in sex hormones are not the same.

The main factors of acute cerebrovascular disease leading to endocrine dysfunction are: 1 gonadotropins related to dysregulation of neurotransmitters: dopamine, norepinephrine and serotonin secretion increase, monoamine metabolism disorder, leading to sex hormones Level changes, estrogen levels are lowered, 2 stress response: the body is in a state of stress and can regulate endocrine by itself.

In addition, many people in the clinic have no cerebrovascular disease even if they have risk factors for cerebrovascular disease, but some people who do not have risk factors for cerebrovascular disease have cerebrovascular disease, indicating that the occurrence of cerebrovascular disease may be related to other factors. Relevant, such as genetic factors and bad hobbies.

Epidemiological studies have confirmed that hyperlipidemia and hypertension are the two main risk factors for atherosclerosis, smoking, drinking, diabetes, obesity, high-density lipoprotein cholesterol, triglyceride increase, serum lipoprotein increase are brain Risk factors for vascular disease, especially risk factors for ischemic cerebrovascular disease.

Brain infarction prevention

For the possible causes, actively prevent and strengthen the prevention and treatment of atherosclerosis, hyperlipidemia, hypertension, diabetes and other diseases.

1. For patients with hypertension, blood pressure should be controlled at a reasonable level, because high blood pressure, easy to cause microvascular hemangioma and atherosclerotic small artery rupture and bleeding; and low blood pressure, cerebral insufficiency, microcirculation stasis It is easy to form cerebral infarction, so it should prevent various factors such as sudden decrease in blood pressure, slow cerebral blood flow, increased blood viscosity, and increased blood coagulation.

2. Active treatment of transient ischemic attacks.

3. Pay attention to mental health, many episodes of cerebral infarction are related to emotional excitement.

4. Pay attention to changing bad habits, moderate physical activity is good for health, avoid bad habits such as smoking, alcoholism, overeating, overeating, mainly low-fat, low-calorie, low-salt diet, and have enough high-quality protein, vitamins , cellulose and trace elements, diet is not conducive to health, mildew food, salted fish, cold food, are not in line with food hygiene requirements, to fast.

5. When the temperature changes suddenly, the air pressure and temperature change significantly, the middle-aged and elderly people, especially those who are frail and sick, are mostly uncomfortable and sick, especially in the cold and summer, the elderly have poor adaptability, reduced immunity, morbidity and death. The rates are higher than usual, so be careful.

6. Pay attention to the signs of cerebrovascular disease in time, such as a sudden side of the face or upper and lower limbs suddenly feel numb, weak and weak, mouth sputum, drooling; suddenly feel dizzy, shaking uncertain; short-term confusion or lethargy.

Comorbid complication Complications, acne, cerebral palsy

1. Characteristic symptoms of pulmonary anxiety response:

1 Sustained tension and anxiety.

2 There are also psychological symptoms, such as inattention, memory loss, sensitivity to the sound and easy irritability.

3 At the same time there are physical symptoms, including sympathetic excitability symptoms, such as elevated blood pressure, rapid heartbeat, chest tightness, rapid breathing, irritability, restlessness, and symptoms of parasympathetic excitation, such as polyuria, increased gastrointestinal activity, infection of the lungs Infection is one of the major complications, and patients with severe bedridden often have pulmonary infections.

2. Upper gastrointestinal bleeding

It is one of the serious complications of cerebrovascular disease, namely stress ulcer, which is caused by the inferior colliculus and brain stem lesions. It is now considered to be associated with the anterior and posterior part of the hypothalamus, the gray nodules and the vagus nerve in the medulla oblongata. Related to the autonomic nerve center in the lower part of the hypothalamus, but its high-level center in the frontal lobe, hippocampus and limbic system, the mechanism of gastrointestinal bleeding is related to the primary or secondary lesions of the above-mentioned sites.

Hemorrhoids

Mainly because the body does not change body position for a long time, and the local skin and tissues are subjected to excessive compression for a long period of time, and a series of manifestations of ischemia and necrosis occur. Patients with cerebrovascular disease have more limbs, limb paralysis, prolonged bed rest, and inconvenient activities. It is easy to compress the bone bulge and other parts, causing local tissue ischemia and hypoxia.

4. Post-cerebral vascular disease depression and anxiety response: Post-cerebral vascular disease depression is a common emotional disorder of cerebrovascular disease, which should be highly valued in clinical practice.

(1) Characteristic symptoms of depression response:

1 The mood is bad, the mood is pessimistic, and the self feels bad. 2 sleep disorders, insomnia, dreams or wake up early. 3 loss of appetite, do not think about diet. 4 Loss of interest and pleasure, lack of motivation for anything, lack of vitality. 5 life can not take care of themselves, self-blame and sin, and passively want to die. 6 weight dropped rapidly. 7 low sexual desire, not even sexual desire.

(2) Characteristic symptoms of anxiety response:

1 Sustained tension and anxiety. 2 There are also psychological symptoms, such as lack of concentration, memory loss, sensitivity to the sound and easy to provoke. 3 At the same time there are physical symptoms, including sympathetic excitability symptoms, such as elevated blood pressure, rapid heartbeat, chest tightness, rapid breathing, irritability, restlessness, and symptoms of parasympathetic excitation, such as polyuria, increased gastrointestinal activity and diarrhea .

Symptoms of cerebral infarction Common symptoms Gait instability, increased intracranial pressure, cerebral ischemia, high fever, coma, muscle paralysis, sensory disturbance, diplopia, mental disorder, nausea

Patients with cerebral infarction are more likely to have atherosclerosis, hypertension, rheumatic heart disease, coronary heart disease or diabetes, as well as smoking, drinking and other bad habits. About 25% of patients have pre-disease History of transient ischemic attack, prodromal symptoms before onset, manifested as headache, dizziness, dizziness, transient limb numbness, weakness, usually slow onset, patients mostly in quiet and sleep, most patients symptoms The disease peaked in a few hours or even 1-3 days.

After the onset of cerebral infarction, most patients are conscious, a small number of different levels of consciousness disorder, general vital signs have no obvious changes, if the brain hemisphere large area infarction, ischemia, edema, can affect the function of the diencephalon and brain stem, onset Shortly after, there is a disturbance of consciousness, even cerebral palsy, death, and if the mind becomes unconscious after the onset, the vertebral-basal artery cerebral infarction should be considered.

1. Main clinical symptoms

The clinical symptoms of cerebral infarction are complex. It is related to the location of brain damage, the size of cerebral ischemic blood vessels, the severity of ischemia, the presence or absence of other diseases before onset, and the presence or absence of other important organ diseases. No symptoms, that is, asymptomatic cerebral infarction; can also be manifested as recurrent limb paralysis or dizziness, that is, transient ischemic attack; severe cases can not only have limb paralysis, death, such as lesions affect the cerebral cortex, in the cerebral vessels In the acute phase of the disease, epileptic seizures may occur, with the highest incidence occurring within 1 day after the disease, while cerebrovascular diseases with epilepsy as the first episode are rare. Common symptoms are:

(1) Subjective symptoms: headache, dizziness, dizziness, dizziness, nausea and vomiting, motoriness and/or sensory aphasia, and even coma.

(2) Cranial nerve symptoms: gaze to the side of the lesion, bilateral facial paralysis and tongue palsy, pseudobulbaric paralysis such as drinking water cough and difficulty swallowing.

(3) physical symptoms: limb hemiplegia or mild hemiplegia, partial sensation diminished, gait instability, limb weakness, incontinence and so on.

2. Clinical classification of cerebral infarction

The infarct size of cerebral infarction is the most lacunar infarction. The clinical manifestations are: subacute onset, dizziness, dizziness, gait instability, limb weakness, a few drinking water cough, difficulty swallowing, but also partiality, partiality Feeling diminished, some patients did not have signs of positioning.

The mid-infarction is characterized by basal ganglia, lateral ventricle, thalamus, bilateral frontal lobe, and temporal lobe. The clinical manifestations are: sudden headache, dizziness, frequent nausea and vomiting, conscious, partial squat, or Partial sensory disturbance, hemianopia, central facial paralysis and tongue, false bulbar palsy, aphasia and so on.

Patients with large infarction have a rapid onset and clinical manifestations are critical. They may have hemiplegia, partial sensation, and even quadriplegia, cerebral palsy, and coma.

(1) internal carotid artery occlusion: internal carotid artery occlusion can be asymptomatic, symptomatic occlusion can cause cerebral artery occlusion similar to the performance of the cerebral artery occlusion, such as contralateral hemiplegia, partial sensation loss, same-direction hemianopia, dominant hemisphere involvement can produce Aphasia, intracranial or extracranial internal carotid artery occlusion accounts for 1/5 of ischemic cerebrovascular disease.

In the case of carotid arteriosclerotic occlusion, nearly 15% of cases have aura, including monocular blindness caused by TIA and ipsilateral retinal artery ischemia. The symptoms of internal carotid artery occlusion are complicated due to the action of the skull base artery ring. Sometimes, the internal carotid artery occlusion may not have focal symptoms, which depends on the compensatory function of the anterior and posterior circumflex vessels such as the anterior and posterior communicating arteries, the ophthalmic artery, and the superficial cerebral artery. It may also be associated with transient blindness and Horner's sign.

(2) Middle cerebral artery occlusion: Since the middle cerebral artery blood supply area is the most common place for ischemic cerebrovascular disease, the clinical signs that occur depend on the affected part.

1 occlusion of the middle cerebral artery: occurs in the proximal middle of the middle cerebral artery, because the entire middle cerebral artery blood supply area is involved, which is the most serious type of cerebrovascular disease in the occlusion of the artery, the clinical aspect of trunk occlusion The performance is caused by contralateral hemiplegia, partial sensory disturbance and hemianopia. The dominant hemispherical artery occlusion may have aphasia, loss of writing, and loss of reading. If the infarct size is large, the severe condition may cause increased intracranial pressure, coma, and brain. Oh, even death.

2 deep cerebral artery occlusion or membranous artery occlusion: can cause contralateral hemiplegia of the lesion, generally no sensory disturbance or unilateral hemianopia, impaired dominant hemisphere, may have aphasia.

3 occlusion of the cortical branch of the middle cerebral artery: it can cause the contralateral hemiplegia of the lesion, with the face and upper limb as the weight. The dominant hemisphere can cause motor aphasia, sensory aphasia, loss of reading, loss of writing, misuse, non-dominant hemisphere can cause Body posture disorder such as lateral side neglect.

(3) occlusion of the anterior cerebral artery: occlusion of the anterior cerebral artery is rare, may be due to embolism from the extracranial or the heart, 1 cortical occlusion: the sensory and dyskinesia of the contralateral lower limb, accompanied by urinary retention.

2 deep perforation occlusion: can cause the contralateral central facial paralysis, tongue tendon and upper limb paralysis, can also occur emotional apathy, euphoria and other mental disorders and strong grip reflex.

(4) occlusion of the posterior cerebral artery: occlusion of the posterior cerebral artery causes ipsilateral hemianopia in the contralateral field, but the macular vision remains, because the bilateral arteries (brain, posterior artery) supply the cortex that innervates the macula, and the middle cerebral artery region The visual defects caused by infarction are different, and the posterior cerebral artery is more serious.

1 Cortical branch occlusion: mainly visual impairment caused by ischemia of the visual pathway, the contralateral side of the lesion is unilaterally blunt or the upper quadrant is blind.

2 deep perforation occlusion: typical thalamic syndrome, lesions of the opposite side of the body with hypothalamic pain, contralateral limb dance-like hyperactivity.

In addition, visual impairment caused by occlusion of the posterior cerebral artery at the midbrain level, including vertical gaze palsy, oculomotor palsy, internuclear ophthalmoplegia, and vertical eye separation, when the posterior cerebral artery occlusion involves the dominant hemisphere occipital cortex The patient presented with a nominal aphasia.

(5) Basal artery occlusion: Since the basilar artery mainly supplies blood of the brainstem, cerebellum, occipital lobe, etc., the clinical symptoms of occlusion of the artery are complicated.

Common symptoms are dizziness, nystagmus, diplopia, cross sputum or cross dysfunction, limb ataxia, quadriplegia, ocular paralysis, dilated pupils, often accompanied by facial nerves, nerves, if the basilar artery is occluded. Trigeminal nerve, paralysis of the vagus nerve and hypoglossal nerve, cerebellar symptoms, etc., severe cases can quickly coma, central high fever, tonic brain, gastrointestinal bleeding, and even death, vertebral-basal artery caused by partial obstruction caused by extensive ventral ventral pons Clinically, the atresia syndrome can be produced. The patient has quadriplegia, no expression, no silence, no speech, but conscious, able to understand people's speech, and understand with eye movements.

(6) Inferior cerebellar artery occlusion: The posterior inferior cerebellar artery mainly supplies the dorsolateral medullary blood. When occlusion, it can cause the medullary lateral syndrome (Wallenberg syndrome), which is characterized by dizziness, nausea, vomiting, nystagmus, and the same side. Loss of feeling, ipsilateral Horner (Horner) sign, difficulty swallowing, hoarseness, ipsilateral limb ataxia, pain in the lower side of the face, lack of temperature, variability of the posterior cerebellar artery, so the inferior cerebellar artery occlusion The clinical symptoms caused are more complicated and variable, but must have two basic symptoms: one side of the posterior group of cranial nerve palsy, contralateral pain, temperature loss disappeared or decreased, before diagnosis.

3. Clinical manifestation type

According to the speed, degree, and stability of the cerebral infarction, the cerebral infarction is divided into the following five types.

(1) Complete cerebral infarction: refers to the peak of the disease within 6 hours after cerebral ischemia, often complete hemiplegia, and the general condition is heavier.

(2) Progressive cerebral infarction: After 6 hours of ischemic attack, the condition is still progressively aggravated. Such patients account for more than 40%, causing many reasons for progress, such as the expansion of thrombus, obstruction of other blood vessels or collateral vessels, and cerebral edema. High blood sugar, high temperature, infection, cardiopulmonary insufficiency, electrolyte imbalance, mostly due to the first two reasons.

(3) Slow progressive cerebral infarction: Symptoms are still progressing within 2 weeks of onset.

(4) Stable cerebral infarction: There is no obvious change in the condition after onset, and it tends to be stable stroke. It is generally considered that the ischemic attack of the internal carotid artery system is more than 24 hours, and the ischemic attack of the vertebral-basal artery system is more than 72 hours. Stable stroke can be considered. In this type of stroke, brain CT scans have more chances of infarction consistent with clinical manifestations, suggesting that brain tissue has irreversible lesions.

(5) Reversible ischemic neurological deficit (RIND): refers to ischemic focal neurokinetic dysfunction recovered within 24 to 72 hours, at the latest within 4 weeks, complete recovery, no sequelae, brain CT Scan for infarct lesions without corresponding sites.

Cerebral infarction

1. Cerebrospinal fluid examination: At present, cerebrospinal fluid examination is not generally performed, and cerebrospinal fluid examination is not used as a routine examination of ischemic cerebrovascular disease. Most patients with cerebral infarction have normal cerebrospinal fluid, such as large infarct size, increased cerebral edema, and increased blood pressure. Sexual infarction may have erythrocytosis, and there may be white blood cells and phagocytosis in the later stage.

2. Hematuria, stool routine and biochemical examination: mainly related to risk factors of cerebrovascular disease such as hypertension, diabetes, hyperlipemia, heart disease, atherosclerosis.

3. Brain CT scan: The main manifestations of brain CT scan of cerebral infarction are:

1 The low density of the lesion: it is an important characteristic manifestation of cerebral infarction, which may be caused by ischemic edema of the brain tissue.

2 local brain tissue swelling: manifested as cerebral sulcus disappeared, cerebral cistern, ventricle compression deformation, midline structure shift to the contralateral side, that is, brain CT scan showed a mass effect, this sign can be observed 4 to 6h after onset.

3 Dense arterial shadow: It is the main brain artery density increase, which is common in the middle cerebral artery. The mechanism occurs because the thrombus or embolus is higher than the density of the contralateral or surrounding brain tissue. Some patients may appear within 24 hours of ischemia.

4. Brain MRI examination: Early detection of cerebral infarction, especially in brain stem and cerebellum, T1 and T2 relaxation time prolonged, T1 in the weighted image showed low signal in the lesion area, T2 showed high signal, brain MRI examination can Small infarcted lesions were found, and brain MRI diffusion imaging can reflect new infarct lesions. MRI has shown advantages in the early diagnosis and differential diagnosis of ischemic cerebral infarction. In recent years, superconducting high-grade magnetic resonance equipment has been put into clinical application. Application of magnetic resonance diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) based on planar echo (EPI) technique for early diagnosis of cerebral infarction, even in acute cerebral infarction, blood perfusion changes and pathophysiological processes The correlation research has made some progress.

5.DSA, MRA, transcranial Doppler ultrasonography: The main purpose of these 3 examinations is to find the cause of vascular disease of cerebrovascular disease. Transcranial Doppler ultrasonography is cheap and convenient, and can find large early detection. Abnormalities of blood vessels (such as anterior cerebral artery, middle cerebral artery, posterior cerebral artery and basilar artery), brain MRA examination is simple and convenient, can exclude vascular lesions of larger arteries, help to understand the location and extent of vascular occlusion, DSA can find Small vascular lesions, and interventional therapy can be applied in time.

Diagnosis and differentiation of cerebral

Middle-aged and elderly people have high blood pressure, diabetes, history of heart disease, etc., when they have a quiet rest, there are signs of nervous system such as hemiplegia, aphasia and other focal neurological dysfunction, or other focal cerebral symptoms, generally no obvious disturbance of consciousness, Should consider the possibility of cerebral infarction, need to do brain CT scan or brain MRI in time to help confirm the diagnosis.

1. Cerebral hemorrhage: more than when the activity or emotional agitation, most have a history of hypertension and blood pressure fluctuations, acute onset, headache, vomiting, disturbance of consciousness more common, brain CT scan can be seen high-density hemorrhage.

2. Brain tumor: slow-progressive cerebral infarction, attention to brain tumor differentiation, primary brain tumor incidence is slow, brain metastasis tumor is sometimes similar to acute cerebrovascular disease, brain CT scan should be done in time, if brain tumor and cerebral infarction can not Identification, it is best to do brain MRI to confirm the diagnosis.

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