What Are Lacunar Infarcts?

Lacunar infarction (LI) refers to small penetrating arteries deep in the cerebral hemisphere or the brain stem. On the basis of long-term hypertension, lesions in the blood vessel wall lead to occlusion of the lumen and the formation of small infarcts. According to statistics, the incidence is quite high, accounting for 20% to 30% of cerebral infarction. Common disease sites include the putamen, caudate nucleus, inner capsule, thalamus and pontine, and a few are located in the radiation crown and subventricular zone of the ventricle. The arteries in these areas are mostly small arteries called deep perforating branches. They are actually the peripheral branches of the cerebral arteries, also called terminal branches. Due to the limited blood supply of deep perforating branches, the obstruction of a single branch only causes a small area of ischemic necrosis of brain tissue, which forms a so-called cavity. Lacunar infarction is a cystic lesion with a diameter of 0.2 to 15 mm, which is multiple. Small infarcts are only slightly larger than the diameter of the blood vessel. After the necrotic tissue is absorbed, the small capsule cavity can remain.

Basic Information

English name

Iacunar infarction

Visiting department

neurosurgery

Common causes

Hypertension arteriosclerosis

Common symptoms

Acute onset with focal neurological dysfunction

Causes of lacunar infarction

Hypertension

The incidence of hypertension in patients with lacunar infarction is 45% to 90%. Long-term hypertension causes degeneration of the arteriolar vascular wall in the brain, narrowing the lumen, and occlusion of the arterioles due to certain hemodynamic factors or the inducement of changes in blood components. The most common cause of lacunar infarction is hypertension arteriosclerosis, especially when chronic hypertension exceeds 21.3 / 12.7kPa (160 / 95mmHg). And the effect of increased diastolic blood pressure on the disease is more obvious.

Arteriosclerosis

Lacunar infarction is closely related to arteriosclerosis. Observations have confirmed that the blood supply arteries of the basal ganglia and inner sac area lesions have severe cerebral arteriosclerosis, that is, segmental arterial structure destruction, fibroid necrosis or vascular necrosis. It has also been found that the obvious changes in the medullary arteries are the hyaline changes of the tube wall and the narrowing of the vascular lumen. The frequency of lacunar infarction in each brain region is directly proportional to the degree of arteriosclerosis.

3. Diabetes

Diabetes can lead to infarcts of small arteries in the distal limbs, kidneys, retinas, peripheral nerves, and cerebral nerves. Blood coagulation and viscosity increase, and platelet adhesion increases during diabetes. Positioning. Epidemiological findings indicate that diabetes is a risk factor for stroke, but there is a lack of evidence linking diabetes and lacunar infarction. Studies have also only confirmed that diabetes is associated with multiple lacunar infarctions and not with single episodes.

4. emboli

(1) Cardioembolic emboli fall off from rheumatic heart disease or non-rheumatic heart disease.

(2) Arterial emboli include atherosclerosis with or without ulcers, fibromuscular vascular disease, and dissection of thrombus in dissection aneurysms. In particular, the emboli formed by the detachment of atherosclerotic plaques in the ascending aorta and carotid arteries is one of the important causes of lacunar infarction, which has caused more and more attention.

5. Other factors

Factors such as hyperlipidemia, hyperviscosity, smoking, drinking, and changes in local blood flow to the brain also affect the occurrence of lacunar infarction.

Clinical manifestations of lacunar infarction

The deep basal ganglia region and the brain stem are important pathways for many nerve fiber bundles to travel, and are the bridge between the brain and the body's nerves. If lacunar cerebral infarction occurs on these pathways, it will cause some nerve conduction to be blocked, resulting in symptoms such as motor, sensory or speech disorders. Because the cavity is small, sometimes it affects motor fibers or sensory fibers alone, and pure motor hemiplegia occurs, or only hemiplegia without hemiplegia appears. However, not all the cavities that occur will cause symptoms, and only those cavities that involve important neural pathways or neural structures will manifest, otherwise there may be no symptoms.

General symptoms include dizziness, headache, numbness, dizziness, memory loss, slow response, convulsions, dementia, unconsciousness, and rare mental symptoms. The main clinical signs are stiffness of the tongue, slower speaking speed, changes in intonation and speech, mild central facial paralysis, hemiplegia of paresis or paresthesia, some pyramidal tract signs are positive, and ataxia is rare.

Lacunar infarction diagnosis

Middle-aged and elderly patients have many years of history of hypertension, acute onset, and focal neurological dysfunction. CT or MRI examination can find corresponding lacunar lesions in the brain, which can be diagnosed.

The diagnostic criteria of lacunar infarction are basically a combination of clinical, pathological and CT scans. The diagnostic criteria of the Fourth National Cerebrovascular Disease Conference of the Chinese Medical Association are:

1. The onset is mostly caused by hypertension arteriosclerosis, which is acute or subacute.

2. Unconsciousness.

3. Lumbar penetrating cerebrospinal fluid has no red blood cells.

4. The clinical manifestations are not serious, and more common manifestations are pure sensory stroke, pure motor hemiparesis, ataxia hemiparesis, articulation insufficiency-hand clumsy syndrome or sensorimotor stroke.

5. Perform CT examinations when necessary to confirm the diagnosis.

Differential diagnosis of lacunar infarction

This disease should be distinguished from lacunar softening caused by small amounts of cerebral hemorrhage, demyelinating disease, cerebral cysticercosis, and metastatic tumors.

Lacunar infarction treatment

Effective control of hypertension and various types of cerebral arteriosclerosis can reduce the possibility of lacunar stroke and is the key to preventing this disease.

Similar to the treatment of atherosclerotic thrombotic cerebral infarction, dehydration is generally not used. Although the prognosis of lacunar infarction is good, it is easy to relapse, so it is especially important to prevent the recurrence of the disease. Various risk factors for cerebrovascular disease should be actively treated for secondary prevention of cerebrovascular disease.

Take the most appropriate treatment according to the patient's age, condition, and underlying diseases; adopt supportive therapy, symptomatic treatment and early rehabilitation; take timely preventive interventions for stroke risk factors such as hypertension, diabetes and heart disease to reduce the recurrence rate and Reduce sickness rate.

Prognosis of lacunar infarction

The prognosis of this disease is good.

Lacunar infarction prevention

Preventive treatment

Preventive treatment should be carried out as soon as possible for clear risk factors for ischemic stroke, such as hypertension, diabetes, atrial fibrillation, and carotid stenosis. Antiplatelet drugs aspirin and ticlopidine can be given, which have a positive effect on the secondary prevention of stroke, and it is recommended to use it; long-term medication should be used intermittently, and those with bleeding tendency should be used with caution.

2. Active prevention for possible causes

(1) The blood pressure of patients with hypertension should be controlled at a reasonable level. Because the blood pressure is too high, it is easy to rupture and bleed the micro-hemangioma and atherosclerotic small arteries in the brain; while the blood pressure is too low, the cerebral blood supply is insufficiency, and when the microcirculation is stagnated, cerebral infarction is easily formed. Therefore, it is necessary to prevent various factors that cause a sudden decrease in blood pressure, slow cerebral blood flow, increased blood viscosity, and increased blood coagulation.

(2) Actively treat transient ischemic attacks.

(3) Pay attention to mental and mental health. Many attacks of cerebral infarction are related to emotional excitement.

(4) Develop good living habits and moderate physical activity is good for health. Avoid bad habits like smoking, drinking, overeating, and overeating. A low-fat, low-calorie, low-salt diet is essential to ensure sufficient quality of protein, vitamins, cellulose and trace elements. Overeating is not good for your health. You must not eat moldy foods, salted fish, or cold foods.

(5) Middle-aged and elderly people, especially those who are frail and ill, should pay special attention to sudden changes in air temperature, obvious changes in air pressure and temperature, and severe cold and high summer seasons to avoid illness.

(6) Pay attention to the precursors of cerebrovascular disease, such as sudden dizziness and shakiness; sudden numbness on the side or upper and lower limbs, weakness, weakness, crooked mouth, drooling; transient unconsciousness or lethargy.