Intracerebral hemorrhage

Introduction to brain bleeding Cerebral hemorrhage (cerebral hemorrhage), also known as cerebral hemorrhage, refers to spontaneous bleeding in non-traumatic brain parenchyma. The causes are diverse. Most of them are caused by rupture of blood vessels caused by hypertension and small arteriosclerosis. Therefore, it is also called hypertensive cerebral hemorrhage. Clinically, hemorrhage of the small arteries in the internal capsule area is the most common. Hemorrhagic hematoma (or blood clot) can split, compress nearby brain tissue, destroy or affect their normal function (sports, sensation, memory, language, mental activity, etc.) and cause hemiplegia, partial numbness, unclear speech, etc. When the amount is large, it causes an increase in intracranial pressure, a shift in brain tissue, and even cerebral palsy. The disease is a common disease. The incidence rate of the elderly over 55 years old is high, and the male is higher than the female. The performance is rapid, rapid development, and early hemiplegia and disturbance of consciousness. Sickness and mortality are high, and it is one of the major diseases that cause human death. basic knowledge The proportion of sickness: 0.74% Susceptible people: good for middle-aged and elderly Mode of infection: non-infectious Complications: Acne, Hypertension

Cause of cerebral hemo

Blood vessels (35%):

Common microaneurysms or microangioma, cerebral arteriovenous malformation (AVM), amyloid cerebrovascular disease, cystic hemangioma, intracranial venous thrombosis, meningeal arteriovenous malformation, specific arteritis, fungal arteritis, smog Disease and arterial anatomy and so on.

Hemodynamics (20%):

There are hypertension and migraine, blood factors such as anticoagulation, antiplatelet or thrombolytic therapy, Haemophilus infection, leukemia, thrombotic thrombocytopenia and so on. Intracranial tumors, alcoholism and sympathetic nerve stimulating drugs. The cause is unknown such as idiopathic cerebral hemorrhage.

Other (10%):

In addition, some factors have a certain relationship with the occurrence of cerebrovascular disease, may be the cause of cerebrovascular disease: 1 blood pressure fluctuations: such as high blood pressure patients have not taken antihypertensive drugs recently, or angry, etc., causing blood pressure to increase, to contract The increase in pressure is especially important. 2 temper or emotional stress: common in angry, after quarreling with people. 3 bad habits: such as smoking, alcohol, excessive salt, overweight. 4 excessive fatigue: such as physical and mental labor, defecation, exercise.

Pathogenesis

1, the mechanism of cerebral hemorrhage

In terms of the mechanism of occurrence, in fact, each case of cerebral hemorrhage is not caused by a single factor, but may be caused by several comprehensive factors. There are many mechanisms for the formation of cerebral hemorrhage in hypertension. It is generally recognized that the theory of microaneurysm is generally considered to be simple. The increase in blood pressure is not enough to cause cerebral hemorrhage, which often occurs on the basis of combined cerebrovascular disease.

(1) rupture of microaneurysm: due to the long-term tension caused by hypertension in the small arterial wall of the brain, an aortic aneurysm is formed in the weak part of the blood vessel wall, and its diameter is generally 500 m. Many arterioles are formed in the intracerebral penetrating artery of hypertensive patients. Tumors, mostly distributed in the striate arteries of the basal ganglia, pons, cerebral white matter and cerebellum, the diameter of the artery is 100 ~ 300m, this aneurysm is formed in the weak part of the blood vessel wall, when the blood pressure suddenly rises, this Cystic blood vessels are easily broken and cause cerebral hemorrhage.

(2) Fat glass-like change or fiber necrosis: long-term hypertension has a damaging effect on the inner membrane of the arterial wall of the brain parenchyma with a diameter of 100-300 m. The lipid in the plasma enters the intima through the damaged endometrium. Wall thickening and plasma cell infiltration, the formation of fat glassy changes, and finally lead to tube wall necrosis, easy to rupture when blood pressure or blood flow changes drastically.

(3) cerebral atherosclerosis: the arterial intima of most hypertensive patients have multiple lesions at the same time, including local fat and complex carbohydrate accumulation, hemorrhage or thrombosis, fibrous tissue growth and calcium deposition, and cerebral atherosclerosis In the case of cerebral infarction, the artery in the ischemic softening zone of the large brain is easily ruptured and hemorrhagic necrotic lesions are formed.

(4) The outer membrane and middle layer of the cerebral artery are structurally weak: the middle cerebral artery is at right angles to the deep perforating-bean vein artery that occurs. This anatomical structure causes sudden increase in blood pressure due to factors such as exertion and agitation. The blood vessel is prone to rupture and bleeding.

2. Pathophysiological mechanism of cerebral hemo

(1) Main pathophysiological changes: blood vessels ruptured to form hematoma, and the surrounding tissues showed cavernous degeneration after 30 minutes of hematoma formation; after 6 hours, the adjacent brain parenchyma changed from time to time with necrotic layer, hemorrhage layer and sponge-like Denaturation and edema.

In addition to mechanical stress, these changes in brain tissue surrounding the hematoma are mainly plasma, and blood cell components such as hemoglobin and other vasoactive substances play an important role.

After hemorrhage, the internal volume of the skull increases, which destroys the stability of the intracranial environment. The resulting cerebral edema leads to further increase of intracranial pressure, and also affects regional cerebral blood flow and coagulation and fibrinolysis system function.

In addition to the space-occupying damage of the hematoma itself, there are blood circulation disorders in the surrounding brain tissue, metabolic disorders (such as acidosis), vasomotor paralysis, damage to the blood-cerebrospinal fluid barrier, and release of various biologically active substances by blood breakdown products. Damage to brain tissue.

1 macromolecular substances: albumin in plasma, cleavage of cell membrane components and macromolecular substances released intracellularly may participate in the formation of cerebral edema.

2 Vasoactive substances in hematoma: The vasoactive substances in the hematoma can diffuse into the brain tissue, causing vasospasm, vasodilation or vascular permeability changes.

3 Some vasoactive substances other than hematoma: such as histamine, serotonin, kinin, bradykinin, arachidonic acid and its metabolites, can aggravate brain tissue damage.

4 free radicals: red blood cell extravasation destruction, hemoglobin decomposition releases iron ions and heme, can induce the production of a large number of free radicals, aggravating brain damage.

5 Active enzyme release: The nerve cells contain a large amount of lysosomes, and various hydrolases are released into the cytoplasm, causing further damage or necrosis of the nerve cells.

6 Endothelin release: Endothelin produced by vascular endothelial cell injury can cause intracellular calcium overload, resulting in vasoconstriction and aggravation of cerebral ischemia.

7 excitatory neurotoxic amino acids: increased excitatory amino acids in the damaged area can promote nerve cell necrosis.

8 Participation of various immune responses: Various chemokines promote the transfer of neutrophils to the lesions, and produce active substances, enzymes and free radicals, which cause direct and serious damage to the local brain tissue.

(2) cerebral edema formation: edema is most serious around the hemorrhage, ipsilateral cerebral cortex, contralateral cortex and basal ganglia also have edema, cerebral edema around the hematoma is both angiogenic and cytotoxic, away from the brain edema of the lesion is As a result of the proliferation of vasogenic cerebral edema, experiments showed that autologous blood injection into the caudate nucleus of mice showed that the edema of the ipsilateral basal ganglia reached a peak within 24 hours, and remained constant until the fifth day began to resolve.

(3) The effect of cerebral hemorrhage on coagulation, anticoagulation, and fibrinolysis status: It is generally believed that tissue thromboplastin is released after acute brain tissue injury, which increases blood coagulation activity, reduces antithrombin consumption, and fibrinolysis. The activity compensatory increase, the study of the coagulation process found that within the first 24 hours after bleeding, the release of thrombin during the formation of clots can cause adjacent brain edema, blood-cerebrospinal fluid barrier disruption and cytotoxicity.

In addition, red blood cell lysis, which peaks about 3 days after the initial bleeding, is another mechanism of brain edema formation, which may be related to the release of free hemoglobin and its degradation products. Recent studies have shown that free radicals, excitatory amino acids and membranes are calcium. Permeability is an important factor in ischemic brain injury. Oxygen free radicals may be derived from arachidonic acid release, catecholamine metabolism, leukocyte activation, nitric oxide synthesis and other pathophysiological processes, and the release of ferric iron. Oxides and hydrogen peroxide are converted to more toxic hydroxyl radicals, a more important neurotransmitter of ischemic cerebral edema, which produces superoxide anions, which are probably associated with blood breakdown products, including three The price is related to iron.

In summary, although the pathophysiological mechanism of cerebral hemorrhage is very complicated, understanding and mastering the pathological process of brain damage during cerebral hemorrhage will contribute to drug therapy and promote the absorption of hematoma and the recovery of nerve function, and at the same time, the cerebral hemorrhage The understanding of pathophysiological mechanisms needs further study.

3. The main pathological changes of cerebral hemorrhage

(1) Hemorrhage site: About 70% of hypertensive intracerebral hemorrhage occurs in the basal ganglia; brain lobe, brain stem and cerebellar dentate nucleus each account for about 10%.

Small intramedullary canal aneurysms are often seen in the deep perforating artery. Hypertensive cerebral hemorrhage is common in the middle cerebral artery. The deep medullary artery (42%), the basilar artery pons (16%), the posterior cerebral artery (15%), the cerebellar nucleus and deep white matter of the superior cerebellar artery branch (12%), the apical occipital lobe and the white matter branch of the temporal lobe (10%), etc., the nucleus hemorrhage often invades the internal capsule and breaks into the lateral ventricle. The blood is filled with ventricular system and subarachnoid space; thalamic hemorrhage often breaks into the third ventricle or lateral ventricle, and damages the internal capsule; pons or cerebellar hemorrhage directly breaks into the subarachnoid space or the fourth ventricle, non-hypertensive cerebral hemorrhage Mostly located under the cortex, common in cerebral amyloid angiopathy, arteriovenous malformation, Moyamoya disease.

(2) pathological examination: swelling of the hemisphere on the hemorrhage, congestion, blood flow into the subarachnoid space or into the ventricles; the hemorrhagic foci form an irregular cavity, the center is filled with blood or purple grape-like blood clots, surrounded by necrotic brain tissue, Bloody softening zone and obvious inflammatory cell infiltration, brain tissue around the hematoma is compressed, edema is obvious, large hematoma can cause brain tissue and ventricle displacement, deformation and cerebral palsy, supratentorial hemorrhage, hematoma down Squeeze the lower part of the hypothalamus and the brainstem to displace, deform and subsequently send out blood. The cerebellum is often present, and the midline structure such as the hypothalamus and the supratentorial brain stem are moved down to form a central iliac crest, such as a high intracranial pressure or a sublingual brain. Large hemorrhage of the stem and cerebellum can occur in the occipital foramen magnum; cerebral palsy is the most common cause of direct death of cerebral hemorrhage

After the acute phase, the blood clots are dissolved, the phagocytic cells clear the hemosiderin and the necrotic brain tissue, the gliosis is proliferated, the small hemorrhagic foci form a glial scar, and the large hemorrhagic foci form a stroke sac.

Cerebral bleeding prevention

Cerebral hemorrhage is also closely related to changes in the weather. When the weather becomes cold, the skin of the human body shrinks, causing a sharp increase in blood circulation in the heart and brain, an increase in cardiac load, an increase in cerebral circulation resistance, and an increase in blood pressure. Therefore, winter is a period of high incidence of cerebrovascular accidents.

Elderly people with high blood pressure, cardiovascular and cerebrovascular diseases, etc., should be especially vigilant in winter to prevent the occurrence of cerebrovascular accidents.

First, life should be regular. The elderly can do some work within their ability, but not too tired.

Second, to control high blood pressure in order to ideally control blood pressure must pay attention to many aspects.

(1) Blood pressure control at an ideal level: Intervention experiments in a large population in China have shown that 140/80mmHg may be the ideal blood pressure value for prevention of cerebrovascular disease, but some people's blood pressure drops to this level and then there are symptoms of cerebral ischemia. The reason may be that the blood pressure is too fast, or the ideal blood pressure for these people is slightly higher than the above value, which is due to individual differences. It is more feasible to gradually lower the blood pressure over a period of time. It is advisable to go to the above level or slightly higher without the symptoms of cerebral ischemia.

(2) The blood pressure should be controlled to be stable: the "peak" and "valley" of blood pressure within 24 hours are close to each other, so as to avoid damage to the blood vessel wall caused by blood pressure fluctuations, and prevent cerebral hypoperfusion caused by low blood pressure, and prevent blood pressure from falling. Too fast.

(3) Maintain a comfortable mood: the occurrence of essential hypertension has obvious relationship with the environment and mental state. Environmental factors include diet, social environment, life change, mental conflict, etc. High stress events can cause sympathetic nerves. Guided vasoconstriction and other autonomic nervous responses have a large and lasting effect on blood pressure. Brod observed that the vasoconstrictor response in hypertensive patients was longer than normal in patients with stress, and the general and special stress response was observed in patients with susceptibility. For acute and long-lasting blood pressure rise, psychophysiological studies suggest that mental stress, autonomic activity and conditional effects can cause high blood pressure. Therefore, supportive psychotherapy for hypertensive patients is necessary.

(4) Simultaneous non-drug therapy: such as limiting salt intake, reducing body weight, lowering blood lipids, moderate exercise, and biofeedback therapy, can consolidate and promote the antihypertensive effect of drugs.

Third, maintain a good attitude to maintain optimism, avoid being too excited, to calm the mind, reduce troubles, sorrows and sorrows, indifferent to fame and fortune, contentment.

Fourth, pay attention to diet and diet should pay attention to low fat, low salt, low sugar, eat less animal brain, internal organs, eat more vegetables, fruits, soy products, with appropriate amount of lean meat, fish, eggs.

Fifth, prevention of constipation dry stool, defecation force, not only increased abdominal pressure, blood pressure and intracranial pressure also rise, it is easy to cause fragile small blood vessels rupture and cause cerebral hemorrhage, to prevent constipation, eat more fiber-rich food Such as green vegetables, celery, leeks and fruits, appropriate exercise and abdomen self-healing massage before getting up in the morning, or with appropriate drugs such as Maren Pill, honey oral, Kaisailu, glycerin for external use; can effectively prevent constipation.

Sixth, to prevent physical exertion and mental work, do not be too tired, overload work can induce cerebral hemorrhage.

Seven, pay attention to weather changes Cold weather is a good season of stroke, vasoconstriction, blood pressure is easy to rise, we must pay attention to keep warm, so that the body adapts to climate change, but also according to their own health, some suitable physical exercise, such as walking, broadcast Gymnastics, etc. to promote blood circulation.

Eight, often left hand daily life, use the left upper limb and the left lower limb, especially the left hand, can reduce the burden of the left hemisphere of the brain, and can exercise the right hemisphere of the brain to strengthen the coordination function of the right hemisphere of the brain, medical research shows that Cerebral hemorrhage is most likely to occur in the right hemisphere with weak blood vessels, so the best way to prevent the occurrence of cerebral hemorrhage is to turn two fitness balls with your left hand in the morning and evening to help the development of the right hemisphere.

Nine, pay close attention to your body changes, strokes will have some aura symptoms, such as no headache, severe headache, dizziness, syncope, some sudden numbness, fatigue or temporary amblyopia, language communication difficulties, etc., should promptly seek medical treatment.

Hemorrhage complications Complications, acne, hypertension

1. Pulmonary infection: Pulmonary infection is one of the main complications of cerebral hemorrhage and one of the main causes of death. Within 3 to 5 days after cerebral hemorrhage, comatose patients often have pulmonary infection.

2, upper gastrointestinal bleeding: is one of the serious complications of cerebrovascular disease, namely stress ulcer, cerebral hemorrhage combined with upper gastrointestinal bleeding, mixed type and internal capsule hemorrhage mostly, accounting for 49% and 36% respectively The mechanism of occurrence is caused by the inferior colliculus and brain stem lesions. It is now thought to be related to the anterior, posterior, gray-white nodules and vagus nerve nucleus in the medulla. The autonomic nerve center is in the lower part of the hypothalamus, but its high-level center is in the forehead. Leaf sputum, hippocampus and limbic system, the mechanism of gastrointestinal bleeding is related to the primary or secondary lesions of the above sites.

3, hemorrhoids: mainly the body does not change the body position for a long time, and the local skin and tissue are subjected to compression for a long time and a series of manifestations of ischemia and necrosis, patients with cerebrovascular disease, due to more elderly patients, limb paralysis, long-term bed rest Inconvenient activity, it is easy to oppress the bone bulge and other parts, causing local tissue ischemia and hypoxia.

4, high blood pressure: common complications after cerebral hemorrhage, pulmonary infection, rebleeding, gastrointestinal stress ulcer, renal failure and multiple organ failure (MOF).

5, post-cerebral vascular disease depression and anxiety response: cerebrovascular disease depression is a common emotional disorder of cerebrovascular disease, clinical should be highly valued, post-cerebral vascular disease depression compared with depression, its depression mood morning light night More severe, less morning and less night, easy to provoke symptoms and anxiety, somatic symptoms are more severe, the degree of depression in the cerebral cortex is significantly worse than those in the subcortical lesions, the degree of depression in the front of the brain Significantly heavier than the latter.

(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 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 and diarrhea .

Symptoms of cerebral hemorrhage Common symptoms Brain death Repeated epistaxis, coma, sensory disorder, partial numbness, high blood pressure, partial loss of speech function

1. Exercise and language barriers

The dyskinesia is more common in hemiplegia, and the speech disorder is mainly characterized by aphasia and verbal ambiguity.

2, vomiting

About half of the patients have vomiting, which may be related to increased intracranial pressure, vertigo, and bloody stimulation of the meninges during cerebral hemorrhage.

3. Disorder of consciousness

It is characterized by lethargy or coma, and the degree is related to the location of cerebral hemorrhage, the amount of bleeding and the speed. A large amount of bleeding in a short period of time in the deep part of the brain, most of them will have disturbance of consciousness.

4, eye symptoms

Pupils often occur in patients with increased intracranial pressure, and may also have hemianopia and eye movement disorders. For example, patients with cerebral hemorrhage often gaze at the bleeding side of the brain during the acute phase.

5, headache, dizziness

Headache is the first symptom of cerebral hemorrhage, often on the head of the bleeding side. When there is increased intracranial pressure, the pain can develop to the entire head. Dizziness is often associated with headaches, especially in the cerebellum and brain stems.

Cerebral hemorrhage

Laboratory inspection

1, cerebrospinal fluid examination: due to the development and application of modern imaging diagnostic techniques, the diagnosis is clear, generally do not do cerebrospinal fluid examination to prevent cerebral palsy, but in the unconditional brain CT scan or brain MRI examination, waist wear still has a certain diagnosis Value, after cerebral hemorrhage due to brain tissue edema, intracranial pressure is generally higher, 80% of patients after the onset of 6h, because the blood can break from the brain parenchyma into the ventricle or subarachnoid space and bloody cerebrospinal fluid, so the cerebrospinal fluid is mostly bloody Or yellow, a small number of cerebrospinal fluid clear, therefore, when the lumbar cerebrospinal fluid clear, can not completely rule out the possibility of cerebral hemorrhage, preoperative dehydration agent should reduce intracranial pressure, there is the possibility of increased intracranial pressure or cerebral palsy, should be taboo Waist wear.

2, blood routine, urine routine and blood sugar: patients with severe cerebrovascular disease in the acute phase of blood routine examination showed increased white blood cells, may have urine sugar and proteinuria positive, cerebral hemorrhage acute blood glucose increased by stress response, blood sugar not only increased Directly reflect the body's metabolic state, and reflect the severity of the disease, the higher the blood sugar, stress ulcer, cerebral palsy, metabolic acidosis, azotemia and other complications, the worse the prognosis.

Film degree exam

1, CT examination: CT scan is the first choice for clinical suspected cerebral hemorrhage, can show a round or oval uniform high-density hematoma, the boundary is clear, and can determine the location, size, shape of the hematoma, and whether it breaks into the ventricle, edema around the hematoma Band and occupancy effect; such as large cerebral ventricle visible high-density cast, ventricular dilatation, ring enhancement around the hematoma after 1 week, hematoma absorption becomes low density or cystic change, CT dynamic observation can find progressive brain Bleeding.

2, MRI examination: can be found in CT can not determine the brain stem or cerebellum small amount of bleeding, can distinguish the cerebral hemorrhage that CT can not identify after 4 to 5 weeks of disease, distinguish between old cerebral hemorrhage and cerebral infarction, showing vascular malformation, According to the dynamic changes of hematoma signal (affected by the change of hemoglobin in hematoma), the bleeding time is judged. 1 Hyperacute period (0~2h): Hematoma is T1 low signal, T2 high signal, and it is not easy to distinguish from cerebral infarction. 2 acute phase (2 ~ 48h): for T1 and other signals, T2 low signal. 3 subacute phase (3 days to 3 weeks): T1, T2 showed high signal. 4 chronic phase (> 3 weeks): T1 low signal, T2 high signal.

3, digital subtraction angiography (DSA): can detect brain aneurysms, cerebral arteriovenous malformations, Moyamoya disease and vasculitis.

4, electrocardiogram examination: patients with cerebrovascular disease because of brain-heart syndrome or the heart itself has diseases, may have changes in heart function and vascular function: 1 conduction block: such as prolongation of PR interval, knot rhythm or atrioventricular separation . 2 arrhythmia: atrial or ventricular premature contraction, 3 ischemic changes: ST segment prolongation, decline, T wave changes, 4 pseudo myocardial infarction ECG changes.

5, dynamic blood pressure test: blood pressure increased significantly within 1 week of acute cerebrovascular disease, higher than the normal reference value, but also higher than the blood pressure level before the onset, suggesting that hypertension is closely related to the onset of acute cerebrovascular disease, meanwhile, Blood pressure fluctuations and hypotension state account for a certain proportion of the incidence of acute cerebrovascular disease. Blood pressure fluctuations can cause blood pressure to rise, and can also be a consequence of high blood pressure, regardless of short-term or long-term blood pressure fluctuations in patients with target organs. Such as the severity of brain damage and the incidence of acute cerebrovascular disease, are significantly increased, blood pressure fluctuations often associated with elevated blood pressure, sudden drop in blood pressure or sudden rise, patients are often accompanied by more obvious symptoms, such as dizziness , headache, syncope, chest tightness, palpitation, etc.

6, transcranial Doppler (TCD): help to determine intracranial hypertension and brain death, when the hematoma> 25ml, TCD shows intracranial hemodynamic asymmetry changes, indicating intracranial pressure asymmetry, pulsation index than average blood flow The speed is more reflective of the asymmetry of intracranial pressure.

Diagnosis of cerebral hemo

diagnosis

Middle-aged and elderly patients suddenly develop symptoms during activities or emotional excitement. Symptoms of focal neurological deficits and symptoms of cerebral hemorrhage such as headache and vomiting should be considered. The combined CT scan can quickly confirm the diagnosis.

Differential diagnosis

1. Identification with other cerebrovascular diseases

Because cerebral hemorrhage and cerebral infarction are different in treatment, the identification of the two is very important. The identification of mild cerebral hemorrhage and cerebral infarction is still difficult. At this time, a CT scan should be performed. For patients with obvious disturbance, the skull should be The occlusion of the internal aorta (such as the middle cerebral artery trunk) is differentiated, in order to distinguish whether it is hemorrhagic or ischemic cerebrovascular disease when the patient's condition permits or is not conditionally CT scan.

2. Identification with brain tumors

Brain tumors generally show a progressive increase in intracranial pressure and neurological localization. According to the medical history, signs, especially combined with brain CT scans, are not difficult to make a diagnosis, but a small number of cases, especially in the elderly, are not typical. In the onset of ischemic cerebrovascular disease, there is no obvious symptom of increased intracranial pressure. Brain CT signs are similar to cerebral infarction, which is easily misdiagnosed. Some patients with brain tumors may suddenly become worse due to intratumoral hemorrhage. The clinical manifestations are similar to the manifestations of cerebral hemorrhage, so it should be highly valued in the clinic. Patients with general brain tumors are actively treated in the clinic. The symptoms may be temporarily improved after the reduction of intracranial pressure, but the general trend is that the disease is aggravating. Therefore, For intracranial high-density lesions, in addition to considering cerebral hemorrhage, the possibility of brain tumors should also be considered, and if necessary, an intensive scan can be performed.

Regarding the cerebrovascular disease caused by brain tumor, that is, brain tumor stroke, and the identification of cerebrovascular disease, the following points can be used as reference: 1 brain tumor stroke is generally not accompanied by hypertension, and cerebrovascular disease has a history of hypertension. 2 Brain tumor strokes are mostly caused by metastases, with the appearance of primary lesions, while cerebrovascular diseases have no associated disease symptoms. After dehydration and symptomatic treatment of 3 brain tumor strokes, the symptoms may be temporarily improved, but the symptoms It will soon be repeated and will be aggravated. After the treatment of cerebrovascular disease is improved, it is generally not repeated. 4 brain tumors have mild hemiplegia and are often accompanied by seizures. Cerebrovascular disease is heavier and the incidence of epilepsy is very high. Low or no, 5 brain tumors, fundus examination, optic disc edema is heavier, and often progressively worse; and cerebrovascular disease optic disc often has no edema or edema, most disappeared soon after treatment, 6 brain tumor strokes more There is a history of increased intracranial pressure such as headache and vomiting, and it gradually worsens. Cerebrovascular disease is mostly acute, and there is no history of increased intracranial pressure. 7 Brain tumor strokes generally have a relatively slow onset. Most of the symptoms are persistent and progressive, while the cerebrovascular disease is relatively acute, the brain CT scan and enhancement, and brain MRI can confirm the diagnosis.

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