Lacunar infarction

Introduction to lacunar infarction Lacunarinfarction is one of the common cerebrovascular diseases. It is a special type of cerebrovascular disease caused by persistent hypertension and small arteriosclerosis. The disease is common in middle-aged and elderly people, more men, and more suffering from hypertension. The disease is common in middle-aged and elderly people, more males, more suffering from hypertension, usually in the acute onset during the daytime activities, solitary neurological deficits often make clinical manifestations, but also gradual onset within hours to days, about 20 % of cases showed a TIA-like onset. basic knowledge Sickness ratio: 0.05% Susceptible people: middle-aged and elderly Mode of infection: non-infectious Complications: Hypertension Depression Affective Disorders Sleep Disorders Insomnia

Lacunar infarction

High blood pressure (25%):

The most common cause of hypertension is the lipid-transformation of small arteries and micro-arterial wall, and the luminal occlusion produces lacunar lesions. It is believed that there is no significant correlation between single-cavity lesions and hypertension, and increased diastolic blood pressure is a multiple cavity. The main cause of sexual infarction.

Thrombosis (30%):

Various types of small embolism such as red blood cells, fibrin, cholesterol, air and atherosclerotic plaques, etc., have been reported in the retinal artery (50 ~ 150m) and cerebral arterioles, the carotid artery extracranial artery Atherosclerotic plaque detachment is the most common source of microemboli, heart disease and fungal aneurysm are also possible sources of emboli; 5 blood abnormalities such as polycythemia, thrombocytosis and hypercoagulable state may also play a role in the disease.

Arteriosclerosis (20%):

Middle cerebral artery and basilar artery atherosclerosis and formation of small thrombus obstruction deep perforating artery can lead to lacunar infarction.

Abnormal blood pressure (20%):

Hemodynamic abnormalities such as a sudden drop in blood pressure cause a significant reduction in blood flow at the distal end of a severely stenotic artery to form a microinfarction.

Pathogenesis

1. Risk factors The mechanism of lacunar infarction is complicated, and there are many problems to be studied. In order to prevent lacunar infarction, it is necessary to identify the risk factors of lacunar infarction. It is generally considered that hypertension, advanced age, diabetes, brain Atherosclerosis, hyperlipidemia, smoking, coronary heart disease, etc. are all important risk factors for lacunar infarction, and the highest incidence of hypertension and lacunar infarction.

(1) Hypertension: Hypertension is a direct and important cause of lacunar infarction. Under the action of hypertension, lipid-transformation occurs in the arterial wall, fibrin necrosis, micro-atheromas and other easily formed cavities. Lacunar infarction, the most important of which is the lamellar infarction caused by lipid hysteresis, Fisher believes that 90% of patients with lacunar infarction have hypertension, domestic data reported in 66.8% ~ 82.4%.

(2) Age: The incidence of lacunar infarction in the elderly over 60 years old is significantly higher than that in young people, especially in the elderly with high blood pressure. Some scholars believe that the age of 45 is more than 10 years old. The risk of lacunar infarction increased by about 1 fold.

(3) embolization embolism: heart disease accompanied by atrial fibrillation, atherectomy of carotid atherosclerosis, etc., due to abundant blood circulation in the brain, embolism is easy to cause lacunar infarction deep in the brain with blood flow, according to reports In 33% of patients with deep lacunar infarction, the cause is derived from embolization of heart disease or carotid atherosclerosis.

(4) Diabetes and hyperlipidemia: Diabetes can cause lipid metabolism disorders, promote and accelerate small atherosclerosis, at the same time, diabetes often associated with hyperlipidemia, increase blood viscosity, slow blood flow, platelet function and Abnormal anticoagulant effect in the body, it is generally believed that capillary disease caused by diabetes and hypercoagulability of blood is an independent risk factor for lacunar infarction.

(5) Transient ischemic attack: It may be a powerful predictor of lacunar infarction. About 28.95% of patients with cerebral infarction have a history of transient ischemic attack 1 to 5 years before onset.

(6) Heart disease: various heart diseases, valvular heart disease accompanied by arrhythmia or heart failure caused by decreased cardiac output, or embolus detachment, can cause the possibility of cerebrovascular disease.

(7) Other:

1 Certain arteritis, non-vascular emboli also have the potential to cause lacunar infarction.

2 bad living habits: such as smoking, alcohol and so on.

3 cervical spondylosis: cervical spine degeneration caused by intervertebral space stenosis, nerve root and vertebral artery compression, so that the vertebral-basal artery blood supply is not enough, easily lead to cerebral ischemic attack.

2. Major pathological changes

(1) Pathological changes caused by hypertension and cerebral arteriosclerosis: Lacunar infarction is a small blood vessel lesion associated with hypertension. Fisher and other patients have long-term hypertension, which can cause small blood pressure. Arteriosclerosis and hyaline degeneration, resulting in vascular occlusion, the lesions of the blood vessels are generally the branches of the main arteries in the brain, such as the anterior cerebral artery, the middle cerebral artery, the posterior cerebral artery and the deep perforator of the basilar artery. These small arteries are 100 in diameter. ~400m, is a terminal branch of cerebrovascular disease, lipid hyaline degeneration occurs in certain segments of the diseased artery, fibrin necrosis, intimal thickening, cellulose-like exudation, microscopic atherosclerosis, narrowing of lumen Then lead to thrombosis or microembolism, can cause vascular occlusion, the formation of small cavity softening lesions, cavity lesions are generally 2 ~ 15mm in diameter, the maximum is not more than 20mm, fresh active lesions can be seen necrotic brain tissue and phagocytic cells, often small arteries Thin wall or visible regenerative small blood vessels, after the necrotic part is removed, regular or irregular cavities appear, which contain liquid, slender connective tissue trabeculae Or a lipid containing macrophages containing hemosiderin, compared with the surrounding dense fiber gum.

(2) Ratio of lacunar infarction to cerebral infarction: In cerebral infarction, the finding rate of lacunar infarction was 10% to 27.8%, and Chamorro found 337 cases of lacunar infarction in 1273 cases of cerebral infarction. 26%, Rothrock found that lacunar infarction accounted for 27% of 500 cases of cerebral infarction, Nadia's 212 cases, 59 cases of lacunar infarction, accounting for 27.8%, PET examination can be found earlier in the local brain tissue The function of the brain changes when the metabolism changes state, so when PET is applied to brain examination, the rate of finding lacunar infarction may be higher.

(3) combined bleeding: lacunar infarction combined with hemorrhage accounted for 35%, may be associated with microaneurysm rupture, that is, hemorrhagic lacunar syndrome.

(4) The location of lacunar infarction: the basal ganglia is more common. Fisher reported that the distribution of the sulcus is 46.8% of the basal ganglia, 15.7% of the brainstem, 13.8% of the thalamus, 12.2% of the radioactive crown, 7.9% of the white matter, and 1.8% of the corpus callosum. Domestic Hou Yuhua et al reported 61.8% of basal ganglia, 15.9% of brain lobe, side ventricle of the lateral ventricle, 11.5% of the semi-oval center, 5.1% of the thalamus, 2.5% and 3.2% of the brainstem and cerebellum, respectively.

(5) Cavity size: The cavity is generally 0.2 to 15 mm, and the cavity larger than 2 cm is called a huge cavity, and the cavity is mostly 2 to 3.

3. Hyperviscosity and lacunar infarction Hyperviscosity is the pathological basis of some ischemic cerebrovascular diseases. Hyperviscosity can increase the microcirculation resistance, causing local blood flow to be slow and stagnant. Ischemia and hypoxia of brain tissue, leading to varying degrees of infarction, hemorheology test, whole blood specific viscosity, plasma viscosity, hematocrit, erythrocyte aggregation and erythrocyte deformation index may affect blood flow structure and blood flow An important factor is the decrease of erythrocyte membrane ATPase activity in hypertensive patients, the abnormal appearance of red blood cell geometry, and the decrease of red blood cell deformability, which is one of the causes of lacunar infarction.

Domestic rhododendron and other studies in patients with essential hypertension with cerebral lacunar lesions imbalance in coagulation and fibrinolysis system suggest that hypertension and cerebral lacunar lesions, there is a rise in von Willebrand factor levels a potential hypercoagulable state caused by high; and a disorder of the fibrinolytic system caused by a change in plasminogen activator, plasminogen inhibitor, and plasminogen activity.

4. Genetic and lacunar infarction In recent years, there have been many reports on genes related to cerebrovascular diseases. Ma Liyuan et al reported in the study of genes related to ischemic cerebrovascular disease that mothers have cerebrovascular disease or transient The incidence of cerebrovascular disease in the offspring is 2.3 times that of no family history. The history of cerebrovascular disease is an independent risk factor for cerebrovascular disease in middle-aged men. When the father suffers from cerebral hemorrhage, his offspring The incidence of cerebrovascular disease is significantly increased, and Hao Jinghua et al. observed angiotensin-converting enzyme gene polymorphism in patients with diabetes mellitus complicated with hypertension. The incidence of lacunar infarction is closely related to type II gene, and type II gene may be Genetic markers and may be predictors of essential hypertension.

Lacunar infarction prevention

Because lacunar infarction is an ischemic cerebrovascular disease caused by deep perforating small artery occlusion, most of these blood vessels are terminal branches. Once the infarction is formed, the collateral circulation is extremely difficult to establish, so the clinical symptoms are mild. , but not easy to recover, should focus on prevention, active treatment of hypertension, hyperlipidemia, diabetes, cervical spondylosis, prevention of atherosclerosis is very important, in the treatment of these diseases, while controlling the bad habits of alcohol and tobacco can not be ignored, about Prevention mainly pays attention to the following points.

1. Active prevention and treatment of hypertension

For middle-aged and elderly people over 40 years of age, blood pressure should be measured regularly to detect high blood pressure and reasonable treatment.

2. Regular blood rheology examination

To observe the dynamic changes of blood viscosity, active treatment of hyperlipidemia and hyperviscosity.

3. Actively change bad habits

Quit smoking, avoid alcoholism, adjust the diet, promote proper sodium intake and adequate potassium-containing foods, eat high-fat foods, and eat more fresh vegetables and fruits.

4. Increase physical activity, maintain a comfortable mood, and reduce the stress intensity of stressful life events.

5. Attaches great importance to the prodromal symptoms of cerebrovascular disease

Such as one side of the face or upper, lower limbs suddenly feel numb, weak and weak, mouth sputum, drooling; suddenly appear difficult to talk or can not understand other people's words; suddenly feel dizzy, shaking, especially dizziness often accompanied by physical symptoms, such as lifting legs Strenuous, walking like stepping on cotton; short-term unconsciousness or lethargy; unbearable headaches, and headaches from intermittent to persistent or accompanied by nausea, vomiting, monocular transient blackness, lasting seconds to several Ten seconds, indicating that the retina has transient ischemia.

6. Effectively control transient ischemic attacks.

7. Timely selection of appropriate auxiliary examination and treatment

Because the disease is not easy to find through special examinations, the above-mentioned changes in the elderly and the elderly are highly valued. They should not be ignored. Actively looking for the causes and treating the risk factors are important measures to prevent lacunar infarction.

Lacunar infarction complications Complications, hypertension, depression, affective disorder, sleep disorders, insomnia

Most patients with lacunar infarction have no obvious complications, but should be alert to various complications of hypertension, and should pay great attention to post-cerebral vascular disease depression and anxiety response, which is a common emotional disorder of cerebrovascular disease.

1. Characteristic symptoms of depression

(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 cannot take care of itself, blame self-crime, and passively want to die.

(6) The body weight drops rapidly.

(7) Low sexual desire, even no 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. Causes diarrhea.

Lacunar infarction symptoms Common symptoms Dizziness Increased intracranial pressure Atherosclerosis Cerebellar ataxia Bean occlusion Arterial trigeminal nerve distribution area Numbness Sense of tinnitus Dementia Positioning dysfunction Sensory disturbance

1. The disease is common in middle-aged and elderly people. There are many males and many people with hypertension. It is usually acutely affected during daytime activities. Isolated neurological deficits often make clinical manifestations obvious, and can also gradually develop in a few hours to several days. About 20% of cases show a TIA-like onset.

2. There are more than 20 clinical manifestations in clinical manifestations. The clinical features are mild symptoms, single signs, good prognosis; no headache, increased intracranial pressure and disturbance of consciousness. It is important to identify lacunar stroke syndrome. Because it can be completely or nearly completely restored.

There are four classic lacunar syndromes in clinical practice:

(1) pure motor hemiparesis (PMH): common, usually the contralateral internal capsule hind limbs or pons lesions, showing facial and upper and lower extremities with the same degree of hemiparesis, without sensation, visual and cortical function loss Aphasia, brainstem lesions do not appear dizziness, tinnitus, nystagmus, diplopia and cerebellar ataxia, etc., more than 2 weeks to begin recovery, PMH can also be occluded by the internal carotid artery or middle cerebral artery, subdural hematoma or brain Caused by endogenous lesions.

There are 7 rare variants in PMH:

1 combined with sports aphasia: due to occlusion of the bean vein artery, the internal capsule knee, hind limbs and adjacent radioactive white matter lesions, without CT confirmed, clinically misdiagnosed as atherosclerotic cerebral infarction.

2PMH without facial paralysis: vertebral artery or deep perforating occlusion leads to one side of the medullary pyramidal microinfarction, which may have mild vertigo, tongue numbness, and lingual muscle weakness.

3 combined horizontal gaze palsy: pathologically confirmed occlusion of the midline artery in the lower part of the pons, involving the median reticular structure near the pons caused a transient one-and-a-half syndrome.

4 combined with oculomotor cross sputum: the middle part of the cerebral peduncle involves the oculomotor nerve efferent fibers.

5 combined with the nerves of the cross: the midline of the lower part of the pons is involved in the lesions of the nerves.

6 accompanied by acute episodes of mental disorder, attention, memory impairment, pathologically confirmed as the forearm of the internal capsule and the anterior part of the hind limb, destroying the thalamus to the frontal lobe.

7 atresia syndrome: quadriplegia, can not speak, the vertical movement of the eyeball is retained, bilateral internal capsule or pons lesions damage the corticospinal bundle leading to bilateral PMH.

(2) pure sensory stroke (PSS): more common, characterized by partial sensation loss, may be associated with paresthesia, such as numbness, burning or heavy feeling, tingling, stiffness, etc.; is the contralateral thalamus The posterior nucleus, the posterior limb of the internal capsule, the posterior part of the radial crown and the dorsolateral lesion of the medulla, the occlusion of the posterior cerebral artery and the small amount of bleeding in the thalamus or midbrain can be similar.

(3) ataxia-hemiparesis (AH): contralateral PMH with cerebellar ataxia, hemiplegia (obvious foot and ankle), upper limbs light, facial lightest; finger nose test, Positive knee-knee test, usually from the upper 1/3 and the lower 2/3 junction of the contralateral pons, the posterior and upper parts of the internal capsule (affecting sputum, occipital bundle and pyramidal bundle) and radial crown and half-egg The center of the circle (affecting the cortical pons and partial pyramidal bundles) is caused by lesions.

(4) dysarthric-clumsy hand syndrome (DCHS): sudden onset, rapid symptoms, peak dysphonia, difficulty swallowing, lesions on the opposite side of the central face, face Inability and fine movements are clumsy, writing is easy to find, finger nose test is not allowed, mild balance disorder, lesions are at the junction of 1/3 and 2/3 of the base of the pons, which is the midline occlusion of the basilar artery; also seen in the internal capsule Knee lesions can be considered as AH variants.

(5) Other syndromes: for example, sensorimotor stroke (SMS), with onset of partial sensory disturbance, recurrence of hemiparesis, lesion in the posterior nucleus of the thalamus and adjacent posterior sac, which is the thalamic geniculate artery Branch or posterior cholangioenteric occlusion of the thalamic branch, lacunar state is a severe lacunar infarction with severe mental disorders, dementia, pseudobulbar paralysis, bilateral pyramidal tract signs, Parkinson's syndrome and urine Incontinence and so on.

3. According to the lacunar infarction, the presence or absence of neurological signs can be summarized into 3 categories.

(1) There are focal neurological localization signs: lacunar cerebral infarction with clear classification, which accounts for about 75% of lacunar infarction.

(2) There are symptoms of the nervous system, but no focal signs, lacunar infarction that can not be classified, accounting for about 9% of lacunar infarction.

(3) No neurological symptoms and signs: about 16% of lacunar infarction.

Lacunar infarction

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. If the infarct size is large, the pressure of cerebral edema may be increased, and a few patients with hemorrhagic infarction may appear. Erythrocyte increase, and there may be white blood cells and cell phagocytosis in the later stage.

2. Hematuria routine and biochemical examination

Mainly related to cerebrovascular disease risk factors such as hypertension, diabetes, hyperlipidemia, heart disease, atherosclerosis, etc., contributing to the diagnosis of the cause.

Other auxiliary inspections:

Brain CT scan

In the early stage of lacunar infarction, especially within 24 hours, CT scan of the brain can not be diagnosed, and only the diagnosis can be ruled out. The best period for the diagnosis of the cavity by CT scan is within 1 to 2 weeks after the onset of the brain. Most of the gaps are low-density, the boundary is clear, the shape is round, elliptical or wedge-shaped, there is no edema zone and space occupying effect, the average diameter is 3~13mm, and the volume of lacunar infarction is small, so CT is The diagnosis rate of the disease is not high. If the detection rate of the lesion is less than 0.5cm, the detection rate is almost zero. Neison et al reported a positive rate of 48.5%. The domestic report CT scan has a lower positive rate for lacunar infarction, and for the cerebellum and brainstem. The lesions in other parts cannot be clearly diagnosed due to the occurrence of more bony artifacts during brain CT scan.

2. Brain MRI examination

MRI shows that lacunar infarction is superior to CT because MRI has high spatial resolution, good tissue contrast, and can detect smaller lesions, and there is no bone artifact on MRI, so the cavity of brain stem and cerebellum Gleural infarction showed clear, MRI and CT diagnosis of cerebral infarction was mainly based on ischemic brain tissue edema, blood-cerebrospinal fluid barrier began to break after 6h ischemia, water and protein leaked from the blood vessels into the infarct area, causing extracellular Angioedema, CT is less sensitive to water, often showing lesions 24 hours after ischemia, and MRI shows cell cerebral edema less than 2 hours after ischemia.

In the diagnosis of early lacunar infarction, MRI has the following advantages over CT:

(1) MRI is more sensitive to water than CT, and early lesions can be found.

(2) Brain CT shows that the lesion depends on the density of the lesion. Although some lesions have a large range, such as tissue density changes are not large, can not be detected by CT, but the water content of the lesion has increased enough to be detected by MRI.

(3) Compared with CT, the resolution of MRI is higher than that of soft tissue. Small lesions can be found. MRI can detect lesions of 1 to 5 mm. CT is difficult to detect lesions with diameter less than 5 mm.

(4) posterior fossa, brainstem, top lesions, CT examination due to the vulnerability of bone artifacts, making the lesion and the surrounding tissue difficult to distinguish, while false positives can occur, while MRI examination has no bone artifacts at all The interference can also be imaged in any direction, thus allowing the lesion to be fully displayed.

(5) MRI is superior to CT in showing the shape, size, number and location of lacunar infarction lesions, which is the first choice for lacunar infarction.

Early lesions: MRI can distinguish between long T1 and long T2 luminal lesions, T2-weighted images are particularly sensitive. According to pathology and MRI, the lesion area of lacunar infarction varies in size from 0.5 to 20 mm. Fisher used to The cavity with a diameter of 10mm or more is called a giant cavity, and then the diameter of the cavity is limited to 20mm. Most scholars believe that the diameter of the cavity should be 15mm. It is reported that the diameter of the infarct can be 40~. 50m, the diameter of the cavity formed can be as small as 0.5mm. For lesions less than 0.5mm in diameter, it should be distinguished from the "screening hole" proposed by Durand Fardel. The "screening hole" is a hole in the medulla that is visible on the cut surface of the brain. There is a blood vessel in each hole, which is the enlargement of the space around the blood vessel, because the hole is small, the brain parenchyma is not obviously damaged, but the retraction of the brain parenchyma is caused. In imaging, especially MRI, it must be Lacunar infarction difference.

3. Cerebrovascular examination

In patients with lacunar infarction, the incidence of carotid artery and skull base artery lesions is high. Doppler ultrasound (TCD), carotid B ultrasound, brain MRA, and cerebral vascular digital subtraction angiography (DSA) should be performed. To determine the cause, nerve intervention can be performed if necessary.

4. EEG topographic map (BEAM)

The EEG topographic map can display the visual distribution of EEG activity in a similar two-dimensional image, which provides useful help for the early diagnosis of lacunar infarction. In cerebral ischemic cerebrovascular disease, there is no obvious morphological aspect. When the brain function is abnormal and the brain function is abnormal, the EEG topographic map can complement the length of the CT and has certain clinical value.

5. Other inspections

Cervical X-ray films, electrocardiogram, cardiac function, cerebral blood flow map and other examinations help to diagnose the cause.

Diagnosis and differentiation of lacunar infarction

diagnosis

The following points can be used as a reference for the diagnosis of lacunar infarction:

1. After the middle age, there is a history of hypertension or TIA, chronic, subacute or acute onset, with mild symptoms.

2. The clinical symptoms are consistent with the above-mentioned clinical manifestations of the lacunar stenosis, and many unconscious disorders.

3. Brain CT scan and MRI examination confirmed the lacunar lesions consistent with the clinical, consistent with the imaging features of lacunar infarction.

4. The prognosis is good and there is a possibility of complete recovery in the short term.

Differential diagnosis

In addition to ischemic infarction, the cause of lacunar syndrome includes small amount of cerebral hemorrhage, infection, cysticercosis (cysticercosis), Moyamoya disease, brain abscess, extracranial carotid artery occlusion, pons hemorrhage, demyelination Diseases and metastases, etc., should be noted for identification.

1. Small focal parenchymal hemorrhage

Due to the small amount of bleeding, hematoma is limited, the onset can be progressive, the clinical manifestations can be similar to lacunar infarction, and must be identified by CT or MRI, but cerebral hemorrhage has its characteristics, that is, cerebral hemorrhage is generally in physical and mental stress activities. Or when the emotion is prone to morbidity, the onset is urgent, the development is fast, and reaches the peak in tens of minutes to several hours. The typical manifestations of acute morbidity are: headache, vomiting, aphasia, limb dyskinesia, convulsions, varying degrees of disturbance of consciousness, brain The clinical manifestations of hemorrhage have a great relationship with the bleeding site and the amount of bleeding. Brain CT scan can find bleeding lesions, which is helpful for differential diagnosis.

2. Giant lacunar infarction

The diameter of the interphalangeal cavity is greater than 20 mm, which may be caused by multiple occlusion arterial occlusions, or larger atherosclerosis or thrombosis. The signs of nervous system localization are more obvious or the symptoms are heavier, may be accompanied by disturbance of consciousness, and the prognosis is poor.

3. Hemorrhagic lacunar infarction

With the wide application of CT, clinicians have found that a small amount of bleeding in the brain can also cause the performance of lacunar infarction. For this type of disease, it is now called hemorrhagic lacunar syndrome. The clinical features are more common in Middle-aged and elderly people over 50 years old, who have a history of hypertension, often have sudden onset of activity, which is progressively aggravated, reaching a peak in half an hour or several hours. There are various similar lacunar infarctions in clinic. The performance, such as simple exercise hemiparesis, simple sensory stroke, ataxia hemiparesis, dysarthria - hand clumsy syndrome, sensorimotor stroke, but due to less brain bleeding, small lesion range, hematoma limitations , did not break into the ventricles and subarachnoid space, did not involve the uplink reticular activation system, generally no headache, dizziness, nausea, vomiting, neck stiffness and other meningeal irritation, no mind, intelligence and pupil changes, it is easy to be misdiagnosed as Lacunar infarction, brain CT scan is the main method of differential diagnosis.

The cause of hemorrhagic lacunar syndrome is mainly caused by hypertension. The lesions are located in the inner capsule, the putamen, the thalamus and the pons. They have a small focal high-density shadow, and the deep arterial wall of the brain is deep due to long-term hypertension. Hardening, fat-like changes, rupture, exudation and onset, hemorrhagic lacunar infarction generally has a good prognosis.

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