Cerebral Embolism
Introduction
Introduction to Cerebral Embolism Cerebral embolism, also known as embolic infarction, refers to some abnormal solid, liquid or gas emboli in the blood circulation of the human body, which enters the cerebral artery or the cervical artery supplying the brain with blood flow. Acute occlusion of the vascular lumen, causing regional cerebral blood flow interruption, resulting in local brain tissue ischemia, hypoxia or even softening, necrosis, so the clinical manifestations of acute brain dysfunction, cerebral embolism often occurs in the internal carotid artery system, vertebra-basal The arterial system is relatively rare. basic knowledge The proportion of sickness: 0.01% - 0.03% Susceptible people: no special people Mode of infection: non-infectious Complications: pulmonary embolism, coronary heart disease, arrhythmia
Cause
Cause of cerebral embolism
Cardiogenic (60%):
The emboli that causes cerebral embolism comes from various heart diseases. Rheumatic heart disease with atrial fibrillation and cerebral embolism ranks first, accounting for more than half; other common ones are: coronary atherosclerotic heart disease with atrial fibrillation, subacute Neoplasms of infective endocarditis, wall thrombus of myocardial infarction or cardiomyopathy, mitral valve prolapse, occlusion of cardiac myxoma and cardiac surgery complications.
About inflammatory substances or neoplasms entering the cerebral blood vessels, which occur on the basis of subacute bacterial endocarditis and congenital heart disease, bacteria adhere to the endocardium of the lesion to multiply, and with platelets, fibrin, red blood cells When it is formed into a bacterial neoplasm, it can cause cerebral embolism with blood flow after shedding. In myocardial infarction, the endocardium of the heart often produces a wall thrombus and falls off into an embolus.
In recent years, the development of cardiac surgery, increased the incidence of some cardiac cerebral embolism, emboli from the systemic venous system, through the congenital heart disease atrioventricular septal defect, directly into the intracranial artery and cause cerebral embolism, called abnormal embolism.
Non-cardiac (30%):
Cerebral embolism caused by non-cardiac emboli has a clear cause, which proves that the embolus is from the heart. The common non-cardiac plugs are mainly the following.
(1) Atherosclerotic plaque detachment: Aortic, carotid or vertebral artery atherosclerosis caused by vascular plaque detachment, resulting in cerebral embolism, in addition to neck large blood vessel trauma, pulmonary vein thrombosis and so on.
(2) Bacterial emboli: For example, in patients with subacute bacterial endocarditis, neoplasms containing a large number of bacteria are often formed on the heart valve, and the sputum is crustaceous and easily detaches into an embolus.
(3) Fat emboli: common in the long bone fractures such as the tibia, femur and tibia or long bone surgery, the fat tissue in the bone marrow is squeezed into the blood to form a fat embolus.
(4) Air emboli: If chest surgery or neck surgery, artificial pneumothorax, pneumoperitoneum, subcutaneous emphysema with vascular injury, air enters the blood circulation to form bubbles, it becomes an air embolus, and there are diving operators. When the hyperbaric oxygen chamber is decompressed too fast when the temperature rises too fast or when the hyperbaric oxygen treatment is performed, the air dissolved in the blood is released, and bubbles are formed in the blood and merged with each other to form an air embolus.
(5) Other embolisms: embolisms such as bronchiectasis, lung abscesses, and infections in other parts of the body (such as lung infections, limb infections, sepsis), tumor emboli formed by tumor material shedding, parasites or insects Eggs, amniotic fluid, etc. can cause cerebral embolism.
Source unknown (10%):
Some cerebral embolisms use modern methods and methods. Although they have been carefully examined, they have not been able to find the source of the emboli, which is called the source of the emboli. Normal human blood is in a fluid state. Although the blood contains macromolecules such as red blood cells, white blood cells, platelets and plasma, they are part of the blood and can pass through the microcirculation through deformation. If blood components such as red blood cells accumulate, The formation of money, it is also easy to block blood vessels.
Pathogenesis
Pathogenesis
Some foreign bodies (called emboli) in the blood circulation of the human body flow with blood flow, such as emboli derived from the heart, the above clots, broken plaques of atherosclerotic plaques, adipose tissue and air bubbles, etc. In the cerebral circulation, the vast majority (73% to 85%) of the emboli enter the internal carotid artery system. Because the middle cerebral artery is actually a direct extension of the internal carotid artery, the middle cerebral artery and its branches are easily affected, and the left brain is the dominant hemisphere. The blood supply is more abundant, so the left middle cerebral artery is most susceptible, the vertebral-basal artery embolization only accounts for about 10%, the anterior cerebral artery embolism is almost no, and the posterior cerebral artery is rare.
Generally, emboli is easy to block the cerebral blood vessels because the blood supply in the brain is very rich, and the brain accounts for 2% of the body weight. Under normal oxygen partial pressure and glucose content, 20% of the total output of the heart enters the cerebral blood circulation. The blood of the brain comes from the carotid artery and the vertebrobasilar system on both sides. The carotid artery mainly supplies the blood in the 3/5 part of the cerebral hemisphere through the internal carotid artery, the middle cerebral artery and the anterior cerebral artery. The vertebral-basal artery system is mainly Blood is supplied to the cerebral hemisphere 2/5 parts of the cerebral hemisphere through the vertebral artery, the basilar artery, the superior cerebellar artery, the anterior and posterior inferior cerebellum, and the posterior cerebral artery.
Rheumatic heart disease associated with atrial fibrillation caused by cerebral embolism: due to valvular lesions, the left atrium is enlarged, the atrial wall, especially the left atrial appendage, muscle contraction is weak, causing blood to flow slowly and congested in the left atrium, in addition, atrial fibrillation causes blood The flow is more likely to produce rotation, and it is easy to form a wall thrombus when rubbed against the rough inner membrane. Especially in rheumatic heart disease complicated with heart failure, there is more chance of forming a wall thrombus. When rheumatic activity is combined with bacterial endocarditis, the heart valve On the inflammatory substances, bacterial neoplasms can fall into the systemic circulation, leading to cerebral embolism. In other non-valvular heart diseases, due to long-term atrial fibrillation caused by myocardial strain and abnormal wall motion, it is easy to form a wall thrombus. When heart failure occurs, blood flow is slow, increasing the chance of thrombosis and shedding.
Thurmann et al analyzed the electrocardiogram of atrial fibrillation, which was defined as gross fibrillation with f-wave amplitude greater than 0.50 mV. The results showed that 87% of patients with rheumatoid V1 lead fibrillation had a rheumatic heart disease, left atrial catheter was measured, and left atrial pressure was increased. X-ray has left atrial enlargement, echocardiography shows left atrial dilatation, indicating that f-wave amplitude of atrial fibrillation is positively correlated with left atrial size, rheumatic heart disease and non-valvular heart disease in left ventricular dysfunction, wall motion In abnormal cases, once atrial fibrillation occurs, there is a great chance of forming a wall thrombus and thrombus detachment. Therefore, actively treating atrial fibrillation and correcting heart failure in time can prevent the formation and detachment of the wall thrombus and prevent cerebral embolism. The key to happening.
2. Pathophysiological changes
When the embolus blocks the cerebral blood vessels, it causes ischemia, hypoxia, brain tissue softening and necrosis. The embolus can be dissolved after a period of time, broken and displaced to the distal end. The original obstructed blood vessels restore blood flow. Due to the increased permeability of the damaged blood vessel wall, a large number of red blood cells may ooze out of the blood vessel, causing blood to ooze out in the original ischemic area, forming a hemorrhagic cerebral infarction, and the brain tissue is likely to cause post-ischemic necrosis because of special brain metabolic activity. Exuberant, the energy demand is the highest, and the brain tissue is almost anaerobic and no glucose storage. The energy is continuously supplied by the circulating blood flow. The normal human brain weighs about 1400g, and the average cerebral blood flow is (50±5)ml/(100g). Brain tissue · min), brain tissue energy required is 33.5J / (100g brain tissue · min), glucose brain consumption is 4 ~ 8g / h, 24h 115g, if the blood is completely interrupted, 8 ~ 12s oxygen depletion, 5min The nerve cells begin to be ischemic and necrotic, so although the ischemia is short, the consequences are serious.
The blood supply to the brain tissue is communicated by the two major systems through the anterior communicating arteries of the anterior cerebral arteries. The middle cerebral artery and the posterior cerebral artery communicate with each other by the posterior communicating artery, forming a cerebral artery ring (Willis ring) at the bottom of the brain. The arterial ring is very important for the regulation and balance of the blood supply system between the carotid artery and the vertebral-basal artery, especially the cerebral hemisphere blood supply, and the formation of the collateral circulation in the pathological state. If the thrombus is gradually formed, the lateral branch The circulation is easy to establish. Because the embolus suddenly blocks the artery, the collateral circulation is often difficult to establish rapidly, causing acute cerebral ischemia in the blood supply area of the artery. When the cerebral blood vessel is locally stimulated by the mechanical stimulation, it can cause different degrees of cerebral vasospasm, so At the onset of cerebral ischemia, the range of cerebral ischemia is more serious, so the clinical symptoms are not only related to the embolization site, but also related to the extent of vasospasm. When the vasospasm is reduced, the embolus is broken, dissolved, and moved. The distal end of the artery, as well as the establishment of the collateral circulation, can lead to a reduction in the extent of cerebral ischemia and a reduction in symptoms.
3. Pathological features of cerebral embolism
Cerebral embolism is common in the internal carotid artery system. The middle cerebral artery is especially common. The vertebral-basal artery system is rare. The pathological changes of cerebral embolism are basically the same as cerebral thrombosis. Because the embolus is often multiple, it is easy to be broken, and there is mobility or possible bacteria. Inflammatory or bacterial emboli), embolic cerebral infarction is mostly multifocal, may be associated with encephalitis, brain abscess, localized arteritis and bacterial aneurysm, fat and air emboli often lead to multiple small embolism in the brain, Parasitic emboli can detect worms or eggs at the embolization site. Except for multiple cerebral infarction, other parts of the body such as lung, spleen, kidney, mesentery, skin and sclera can also find evidence of embolism. Cerebral ischemia caused by cerebral vasospasm is more serious than thrombotic cerebral infarction.
The incidence of cerebral embolism with hemorrhagic infarction (spot oozing) is about 30%. Because of blood oozing, hemorrhagic cerebral infarction is also called red cerebral infarction. Red cerebral infarction often indicates cerebral embolism. This may be due to embolus. Temporary occlusion of the aorta caused by ischemic deformation or even necrosis of the vessel wall. When the embolus is decomposed, the small embolus flows to the distal small artery, and the permeability of the vessel wall is enhanced due to damage of the vessel wall at the original embolization. When the blood flow is restored, it is prone to oozing. The extent of pathological damage is often larger than that of the same cerebral atherosclerotic ischemic infarction, probably because the rate of cerebral embolism is higher than that of atherosclerotic brain. The infarct is fast, and the collateral circulation is difficult to establish immediately.
Prevention
Cerebral embolism prevention
Mainly for possible causes, early diagnosis, early treatment, and active prevention.
Prophylactic treatment for risk factors such as hypertension, diabetes, atrial fibrillation and carotid stenosis with clear ischemic stroke, antiplatelet drug aspirin 50 ~ 100mg / d, ticlopidine 250mg / d, It has a positive effect on secondary prevention of stroke, and is recommended for application; there should be a discontinuous period in long-term medication, and those with bleeding tendency should be used with caution.
1. Patients with cerebral embolism have a great chance of embolization, so it is necessary to take preventive measures, atrial fibrillation and hypertension, or patients with diabetes or heart failure, implanted artificial heart valve, mitral stenosis and chronic rheumatic heart disease. Patients with atrial fibrillation are also at high risk, and preventive measures should be taken even if cerebral embolism does not occur.
2. A number of large-scale clinical trials have clearly demonstrated that adjusted doses of oral warfarin can reduce cerebral embolism in high-risk populations by 2/3, patients with chronic rheumatic heart disease with mitral stenosis, and those with artificial heart valves should take oral warfarin. The efficacy of aspirin is far less than that of warfarin, but the use of warfarin must strictly control the degree of anticoagulation.
Complication
Cerebral embolism complications Complications pulmonary embolism coronary heart disease arrhythmia
1. Because the embolus flows along the bloodstream, depending on the location of the flow, it can cause the infarction of the corresponding organ, so there are often signs of embolism in other parts of the clinic, such as pulmonary embolism (air urgency, cyanosis, chest pain, hemoptysis and pleural friction sound, etc.) , renal embolism (low back pain, hematuria, etc.), mesenteric embolism (abdominal pain, blood in the stool, etc.), skin embolism (bleeding point or ecchymosis) and other symptoms, signs.
2. Most patients are also associated with rheumatic heart disease, coronary heart disease and severe arrhythmia, or cardiac surgery, long bone fractures, and other clinical manifestations after endovascular intervention.
Symptom
Symptoms of cerebral embolism common symptoms cerebral ischemic foci localization signs hyperthermia double vision ataxia transient cerebral ischemia convulsion atherosclerotic sensory disturbance
Different from the onset of cerebral arteriosclerotic cerebral infarction, it is generally considered that the onset of cerebral embolism is acute and the condition is serious. It may be because the detached embolus suddenly blocks the cerebral blood vessels, the collateral circulation is too late to establish, and the brain tissue has no slow ischemia adaptation process. Infarction often occurs at the beginning of the middle artery and can cause large cerebral infarction. The main clinical features are as follows.
1. General information
(1) About the age of onset: Because of the different sources of embolism, the age of onset of cerebral embolism is also different. For example, those with rheumatic heart disease are mainly young and middle-aged. If coronary heart disease, myocardial infarction, arrhythmia, atherosclerosis Hardened people are more common in the elderly.
(2) often have symptoms and signs of primary disease that cause emboli origin, and may even be associated with symptoms or signs of embolism of organs other than the brain, such as rheumatic coronary heart disease with atrial fibrillation, clinical manifestations of myocardial ischemia, subacute Infective endocarditis may have fever, joint pain, chest tightness, chest pain in myocardial infarction, fat embolism may have long bone fractures.
2. Incidence
Acute onset is the main feature, and it is one of the most urgent diseases. Most patients do not have any prodromal symptoms before the disease. Sudden onset during the activity, most of the symptoms develop to the highest peak in a few seconds or minutes, a small number of patients In a few days, there is a step or progressive deterioration, and about half of the patients have a disturbance of consciousness at the onset, but the duration is short.
3. Neural system positioning signs
Most of the cerebral embolism occurs in the internal carotid artery system, especially the middle cerebral artery. The neurological dysfunction caused by embolization depends on the number, extent and location of the embolism. There may be headache, dizziness or localized pain during acute onset.
(1) middle cerebral artery embolization: the most common, its clinical manifestations of main embolism caused by contralateral hemiplegia, partial sensory dysfunction and hemianopia, dominant hemispherical artery embolization may have aphasia, loss of writing, loss of reading, such as large infarct size When the condition is severe, it can cause increased intracranial pressure, coma, cerebral palsy, and even death; deep cerebral artery or membranous artery embolization can cause contralateral hemiplegia of the lesion, generally no sensory disturbance or unilateral hemianopia, impaired dominant hemisphere There may be aphasia, cortical embolism of the middle cerebral artery can cause contralateral hemiplegia of the lesion, with the face and upper limbs as the weight, the dominant hemisphere can cause motor aphasia, sensory aphasia, loss of reading, loss of writing, misuse; non-dominant hemisphere Can cause contralateral side neglect and other physical obstacles, a small number of patients may have focal epilepsy.
(2) When the anterior cerebral artery is embolized, the sensory and dyskinesia of the contralateral lower limb can be produced. The contralateral central facial paralysis, the lingual tendon and the upper limb paralysis can also cause emotional apathy, euphoria and other mental disorders and strong grip reflex. With urinary retention.
(3) Post-cerebral arterial embolization can cause contralateral unilateral blindness or upper quadrant blindness, contralateral hemifacial sensation with thalamic pain, contralateral limb dance-like hyperactivity, various ophthalmoplegia and so on.
(4) The most common symptoms of basilar artery embolization are dizziness, nystagmus, diplopia, cross sputum or cross dysfunction, limb ataxia. If the basilar artery is embolized, quadriplegia, paralysis of the eye muscles, dilated pupils, often With facial nerve, nerve, trigeminal nerve, vagus nerve and hypoglossal nerve palsy and cerebellar symptoms, severe cases can quickly coma, quadriplegia, central high fever, gastrointestinal bleeding and even death.
Examine
Examination of cerebral embolism
Laboratory inspection
1. Cerebrospinal fluid (CSF) Checking normal brain pressure, increased brain pressure suggests large area cerebral infarction, hemorrhagic infarction CSF can be bloody or microscopic red blood cells; infectious cerebral embolism such as subacute bacterial endocarditis, CSF cell number increased (200 ×106/L or more), mainly neutrophils in early stage, mainly in late lymphocytes; fat spheroids can be seen in fat embolized CSF.
2. The routine and biochemical examination of hematuria is mainly related to infections with possible emboli, rheumatic heart disease, coronary heart disease and severe arrhythmia, or cardiac surgery, long bone fracture, endovascular intervention, etc. Others can be selected according to the patient's condition. Blood pressure, diabetes, hyperlipidemia, atherosclerosis and other aspects of the examination.
Film degree exam
The purpose of the examination is to not only determine the location of the cerebral embolism, the extent of edema, or the presence or absence of bleeding, but also to find the source of the embolus, such as cardiogenic, angiogenic and other sources of emboli, that is, clear cerebral embolism The cause.
1. Auxiliary examination for cerebral embolism
(1) Brain CT scan: The CT scan of the brain is similar to that of cerebral infarction, that is, after 24 to 48 hours after onset, the CT scan of the brain shows that there is a low-density infarction in the embolization site, the boundary is not clear, and there is a certain occupancy effect, which is done within 24 hours. Brain CT scan, cerebral embolism can be a negative result, that is, brain CT scan negative in this period can not rule out cerebral embolism, brain CT scan has a greater value for clear infarct size, size and peripheral cerebral edema, if it is hemorrhagic infarction, High-density hemorrhage can be seen in the low-density foci. Brain MRI should be selected for the early stage of the disease and the suspected lesion in the posterior fossa or lesion.
(2) Brain MRI examination: early detection of infarction and small embolization lesions, brain MRI examination of brain stem and cerebellar lesions is significantly better than brain CT scan, brain MRI examination can detect ischemic sites earlier, especially brain stem And the cerebellar lesions, 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 find smaller infarct lesions, brain MRI diffusion imaging can reflect new infarct lesions Diffuse MRI is diagnosed according to the diffusion coefficient of the non-invasive measurement molecule in the living body, because the water content in all infarcts increases, and in the diffuse MRI, the surface diffusion coefficient of water molecules in the chronic infarct increases, so it shows a low signal. .
(3) DSA, MRA, transcranial Doppler ultrasonography: is the cause of vascular disease in cerebrovascular disease, can suggest embolization of blood vessels, and display lesions such as vascular stenosis, atherosclerotic ulcer, endothelium Rough and other conditions, transcranial Doppler ultrasonography is cheap, convenient, and can detect abnormalities of large blood vessels (such as anterior cerebral artery, middle cerebral artery, posterior cerebral artery and basilar artery). Brain MRA is simple and convenient. It can rule out vascular lesions of larger arteries, help to understand the location and extent of vascular occlusion, DSA can detect small vascular lesions, and can apply interventional therapy in time.
(4) EEG topographic map, EEG, etc.: These tests have no specific changes, abnormal radio waves can occur at the embolization site, but negative ones cannot exclude cerebral embolism.
2. Auxiliary examination for the source of the embolus
(1) ECG or 24h dynamic electrocardiogram: can understand whether there is arrhythmia, myocardial infarction and so on.
(2) echocardiography: can understand heart valve disease, mitral valve prolapse, endocardial lesions, myocardial conditions.
(3) Carotid ultrasound examination: can show the common carotid artery and internal and external carotid artery with or without atherosclerotic plaque and stenosis.
(4) X-ray examination: chest X-ray examination can find chest diseases such as pneumothorax, lung abscess and heart enlargement, and if necessary, chest CT scan.
(5) Fundus examination: mainly the manifestation of retinal atherosclerosis in the fundus, and sometimes the fundus arterial thrombosis can be found.
(6) Other examinations: Different examinations such as kidney examination and bone examination can be selected according to the possible sources of the embolus.
Diagnosis
Diagnosis and differentiation of cerebral embol
diagnosis
1. The onset of abruptness is mostly without prodromal symptoms, and the onset is rapid. In seconds, the disease often peaks within a few seconds after onset.
2. Most patients have signs of nervous system such as hemiplegia, partial sensory disturbance and hemianopia. In the main hemisphere, there are motor aphasia or sensory aphasia. A few patients have dizziness, vomiting, nystagmus and ataxia, and may have transient loss of consciousness. , or limited or generalized convulsions, severe patients can have coma, gastrointestinal bleeding, cerebral palsy, and even death soon.
3. Diseases with emboli origins Most patients have emboli-derived diseases such as heart disease, atrial fibrillation, cardiomyopathy, myocardial infarction, etc., especially the symptoms and signs of atrial fibrillation.
4. Brain CT scan or MRI examination 24 hours after 48 hours after onset, CT scan of the brain showed a low-density infarct in the embolization site, the boundary was not clear, and there was a certain occupancy effect, but the brain CT scan negative within 24 hours could not rule out cerebral embolism. Brain MRI can detect infarcts and small embolization lesions earlier, and MRI examination of brain stem and cerebellar lesions is better than brain CT scan.
Differential diagnosis
The disease often needs to be differentiated from acute cerebrovascular disease such as atherosclerotic cerebral infarction, cerebral hemorrhage, subarachnoid hemorrhage, and brain CT scan is helpful for the identification of hemorrhagic cerebrovascular disease and ischemic cerebrovascular disease, but for Cerebral embolism caused by fragmentation of carotid atherosclerotic plaque, clinical brain CT scan or MRI examination are not easy to identify with atherosclerotic cerebral infarction, should be carefully asked about the history and careful examination to distinguish.
Atherosclerotic cerebral infarction
Atherosclerotic cerebral infarction and cerebral embolism are ischemic cerebrovascular diseases, which are collectively referred to as cerebral infarction. The symptoms are similar and often confused, but the causes are different.
(1) atherosclerotic cerebral infarction occurs mostly after middle age, the onset is slow, often reaches a peak in a few hours or days, usually there are aura symptoms before the onset, and the age of onset of cerebral embolism is uncertain, many without predecessors Symptoms, rapid onset, a few seconds to 2 to 3 minutes, there are clear signs of nervous system positioning.
(2) atherosclerotic cerebral infarction is caused by stenosis or occlusion of the cerebral blood vessels itself, resulting in ischemia, softening, necrosis of the brain tissue, a series of central nervous symptoms such as hemiplegia, aphasia, sensory disturbance, etc., and cerebral embolism is due to The cerebral blood vessels are caused by obstruction of solids, gases, liquids and other emboli caused by blood flow, and the cause is mostly outside the cerebral circulation.
(3) atherosclerotic cerebral infarction often occurs in a quiet and sleep state. After waking up, I find that I can't move or aphasia freely. Before the onset of cerebral embolism, there is often a history of strenuous exercise and emotional agitation.
(4) atherosclerotic cerebral infarction often has hypertension, arteriosclerosis, transient ischemic attack, diabetes and other medical history, cerebral embolism has a variety of previous medical history, mainly seen in rheumatic heart disease, coronary heart disease and other combined atrial fibrillation Wait.
(5) atherosclerotic cerebral infarction with hemiplegia and language disadvantage as the main symptoms, multiple unconscious disorders or headache, vomiting, etc., cerebral embolism often after headache, vomiting, disturbance of consciousness, aphasia, hemiplegia and other clinical manifestations.
2. Hemorrhage
Cerebral hemorrhage and cerebral embolism Although the symptoms of the nervous system are similar, there are two different types of cerebrovascular diseases.
(1) cerebral hemorrhage usually occurs when emotional, physical activity or concentrated mental work, cerebral embolism is caused by heart disease, arteriosclerosis and other embolism caused by detachment, there is no incentive before the disease, cerebral embolism is more acute.
(2) Progress of the disease: Although the condition of the cerebral hemorrhage progresses rapidly, it can occur within a few minutes, but most of them progress for several hours, while the cerebral embolism is usually in the seconds to minutes, so the latter is faster. .
(3) cerebral hemorrhage often has a history of hypertension, and cerebral embolism often has heart disease, especially heart disease with atrial fibrillation or other sources of emboli.
(4) Brain CT scan can confirm the diagnosis.
3. Subarachnoid hemorrhage
Subarachnoid hemorrhage is also a rapid onset of cerebrovascular disease, which is not easy to distinguish from cerebral embolism, but subarachnoid hemorrhage is a rapid onset, but often accompanied by severe headache, mostly tearing or severe pain, frequent Vomiting, in addition to the positive meningeal irritation, there are generally no other signs of nervous system localization, that is, generally do not cause limb paralysis, some patients have irritability, convulsions, hallucinations and other mental symptoms, or accompanied by convulsions and coma, early brain CT scan showed high density of blood shadow in the subarachnoid space or ventricle. The lumbar puncture examination was uniform and consistent with blood cerebrospinal fluid. The pressure increased and the subarachnoid hemorrhage was divided into two types:
(1) Primary subarachnoid hemorrhage is caused by rupture of blood vessels on the surface of the brain and the bottom of the brain, and blood directly flows into the subarachnoid space. The most common cause of clinical subarachnoid hemorrhage is congenital intracranial artery. Tumor and vascular malformations.
(2) Secondary subarachnoid hemorrhage is caused by hemorrhage of the brain parenchyma, which is caused by blood penetrating into the subarachnoid space or from the ventricular system into the subarachnoid space.
The identification of the two mainly relies on brain CT scan.
