Encephalomalacia

Introduction Brain softening: Because the brain tissue is extremely high in oxygen, once the artery is blocked, it will inevitably lead to softening of the supply area, and brain softening is the infarction of other organs. The larger one is softened, the smaller one is a cavity, and most of the cavity is called a cavity state. Causes of softening and lacunar state are embolism, arterial thrombosis, arterial spasm, circulatory insufficiency and other causes. Softening can be divided into anemia and hemorrhagic. Arterial occlusion can cause anemia softening, and it can also be hemorrhagic softening, while venous obstruction is almost completely hemorrhagic softening. The process of anemia-softening lesions can be roughly divided into three phases: necrosis, softening, and repairing. The cells in the softened zone have been necrotic, and the ischemic penumbra (half-moon zone) has a cell apoptosis or pre-apoptotic state, and its function is low, and neurological and motor system dysfunction can occur.

Cause

The supply of arteries in the brain is extremely abundant, and the collateral circulation is also good. Therefore, from the anatomical point of view, any small arteries in the brain are not terminal arteries. But from a functional point of view, these are indeed the final arteries. Because the brain tissue is extremely high in oxygen, once the arteries are blocked, it will inevitably lead to softening of the supply area, and brain softening is also the infarction of its organs. Softening is divided into large softening and small softening depending on the size and the blood supply of the arteries. Most of them are lesions in the blood supply field of the cerebral aorta such as the internal carotid artery, mostly in the cortex of the cerebral hemisphere and its white matter, while the small one is small. Arteries, such as the occlusion of the middle cerebral artery or vertebral-basal artery, are mostly distributed in the hypothalamus, the basal ganglia and the upper part of the brainstem. Some scholars say that the larger one is softening, and the smaller one is a cavity. Most of the cavities are called cavities. status. There are many reasons for the softening and lax state.

1. Embolization: In the past, it was thought that softening was caused by thrombosis. In recent years, many have proved that most of the softening is at least 50%-60% due to embolism. The source of emboli is mostly the wall thrombus in the heart, the neoplasm or intracardiac myxoma, and the atherosclerotic plaque of the aorta. It can also be a tumor embolus for malignant tumor and a fat embolus at the time of fracture.

2. Arterial thrombosis: The causes include various arterial lesions described in the previous section, the most common being atherosclerosis, followed by various arteritis, and atherosclerotic plaques can also fall off in addition to occluding arterial thrombosis. Causes embolism.

3. Arterial spasm: Generally, normal arteries are not prone to spasms, and atherosclerotic arteries are less prone to spasms. Angiography confirmed that primary subarachnoid hemorrhage, meningitis and angiography can cause cerebral vasospasm, which in turn causes insufficient or softening of blood supply to the brain, which can be caused by stimulation of blood decomposition products or iodine.

4. Incomplete circulation: common in all types of shock. Such as

1 Low volume shock due to blood loss or loss of water.

2 Cardiac shock due to reduced blood output in acute heart failure.

3 septic shock. Sometimes, due to autonomic degeneration or dysfunction, transient hypotension can also occur. This hypotensive state is not harmful to a person with a normal cerebral artery, but if a certain cerebral artery causes softening in the blood supply range of the artery. Sometimes the degree of hypotension is heavy and lasts for a long time. Even if the cerebral artery is normal, it can soften at the junction of the middle cerebral artery and the anterior or middle cerebral artery and the posterior cerebral artery, which is called softening at the junction. Another form of circulatory insufficiency is steal syndrome. If the proximal left subclavian artery is blocked before the vertebral artery is released, the upper limb will increase blood supply during strenuous exercise, and the blood will be vertebral artery. Retrograde flow into the distal part of the subclavian artery causes symptoms of ischemia of the vertebral-basal artery.

an examination

Related inspection

Brain ultrasound examination of brain CT examination of brain MRI

EEG and brain CT examinations are required.

In patients with atherosclerosis, transient ischemic attack often occurs, which is characterized by transient single-limb or hemiparesis, limb sensory disturbance or aphasia, and complete recovery within 24 hours. In the past, clinicians thought that it was caused by cerebral vasospasm, but the hardened arteries were not prone to paralysis, so this explanation is not acceptable. According to meticulous clinical observations, combined with the advent of CT and the continuous exploration of autopsy work, it is now believed that this short episode, due to the temporary blockage of a small artery by a small embolism, causes dysfunction, but has not caused tissue necrosis. The embolus has fallen off. As the author had encountered a patient, the left eye suddenly became blind, and a glass-like embolus in the left axillary arteriole was found during the examination. After a few hours, the patient recovered vision and the fundus was completely normal. The other part, probably due to the formation of a small softening lesion, but far away from important structures such as the inner capsule or ascending sensory fibers, the slight edema caused by compression of these fibers disappears within a few hours, so the function is fully restored, but the softening is still present.

The recent application of CT has greatly helped explain this phenomenon. If a patient has a hemiplegia in his medical history, CT may have found 3 softening lesions, indicating that the other two did not cause symptoms. Sometimes patients have never had a stroke, and CT can find 2 or 3 softening lesions. The autopsy workers actually noticed that some patients died as a result of a stroke, but two other old softening lesions were found in the brain. Explain that the lesions in these quiet areas, if close to important structures, may cause a brief episode of the patient due to edema, which proves that many so-called transient ischemic attacks are not without pathological basis. Another so-called reversible ischemic nervous system dysfunction, which is a neurological dysfunction such as monotherapy, sensory disturbance, aphasia, etc., completely recovered within 3 weeks. The symptoms are caused by softening close to important structures. The author encountered a patient with sudden left hemiplegia and complete recovery in 3 weeks, but CT found a softening lesion in the right nucleus, which further indicates that the so-called transient reversible cases are actually caused by softening lesions, and their pathology. basis. As long as the clinician understands the pathogenesis, these terms can be retained and benefit the patient's psychological comfort. In 1993, Fries et al reported that the patient's internal capsules were fully recovered after softening of the hind limbs. He used magnetic resonance imaging to find that the hind limbs of the internal capsule did soften. This is another powerful indication that the brain has a complete compensatory function.

Differential diagnosis

Softening can be divided into anemia and hemorrhagic. Arterial occlusion often causes anemia softening, and may also be hemorrhagic softening, while venous obstruction is almost completely hemorrhagic softening. The process of anemia-softening lesions can be roughly divided into three phases: necrosis, softening, and repairing.

1. Necrotic phase: It is not easy to distinguish from the normal surface of the brain. The necrotic part may be slightly swollen and the meningeal blood vessels are highly congested. The cut surface is slightly raised and may be slightly harder than normal.

2. Softening period: After several days, the lesion area is obviously soft, the cut surface is light yellow, and the gray matter and white matter are unclear.

3. Recovery period: the lesion area tends to be concave, the larger one is often cyst-like, the wall may be smooth, containing clear or turbid liquid, or it may be a multi-atrial shape formed by a bundle of fibrous capsules with different vertical and horizontal directions. . The smaller one is lacunar. Smaller ones may be harder scar tissue.

Observation under the microscope: The recent observations of the authors are quite different from those in the past books. I will describe them under the microscope and observe the different performances of 30 fresh anemia softening in four weeks. Ischemic neurons disappeared completely on the 16th day; pale nerve cells - pure pulp with only a small number of nuclei can still be seen - that is, the so-called ghost cells in the past - from the second day, until the 19th day It can be seen that necrotic glial dendritic cells appear from the first day to the 15th day; the degeneration of myelin and axonal can be seen from the first day to the 27th day; The nucleated white blood cells can be seen on the first day and disappear on the sixth or seventh day. The plaque cells appeared from the 5th day and gradually increased on the 27th day; the hemosiderin was still from the 8th day to the 19th day; the newly produced blood vessels began from the 4th to 5th days, and the 27th day Have. From the above data, the new necrotic phase should be 4 weeks instead of 1-2d. The so-called second softening period is replaced by lattice cells and astrocytes and fibers at the edges. The recovery period of the third phase is mainly composed of astrocytes and fibers. At this time, the lattice cells have been greatly reduced, and only a few are occasionally between the glial fibers, and some may contain hemosiderin. The ratio of astrocytes to fibers is often determined by the duration of time. The longer the time, the more fibers and the fewer cells, forming a heterogeneous gel-like change. Secondly, the common connective tissue and blood vessels from the blood vessels, in addition to participating in the formation of scars and cyst walls, often form a septum within the capsule. Sometimes, although there is no cyst in the general examination, a small gap can be seen under the microscope. The first layer of the cortex (molecular layer) is often unaffected, with only astrocytes proliferating, and the following cortical softening shapes are juxtaposed with a complete first layer and the following two or three layers of mosaic state. The reason why the molecular layer is not damaged is that the layer is not supplied by the cerebral aorta, but is supplied by the meningeal artery, so it is well preserved.

The above is anemia softening, when the spotted blood vessels in the peripheral blood vessels of the lesion area increase, a larger hemorrhagic foci can be formed, which is more common in gray matter. Most scholars believe that hemorrhagic softening is often caused by embolism. Because of the sudden onset of softening, peripheral blood vessels can easily flow blood outside the damaged blood vessels. Another mechanism of formation is Adam. The embolus enters the artery and blocks the artery. Soon the artery is loosened by hypoxia. The embolus is rushed to the distal end by the blood flow. The softening of the lesion and its surrounding tissue causes massive bleeding. This creates a hemorrhagic softening foci that also contains a small anemia softening foci that prevents bleeding from entering the distal artery. This type is theoretically very reasonable but actually very rare. The author has not seen a typical such lesion for 40 years. It can be confirmed that most of the hemorrhagic softening is caused by embolism, and thrombosis is less common. Another type of arterial hemorrhagic softening is formed by the obstruction of intermittent arteries. For example, one side of the cerebral hemisphere is swollen in the cerebellar stenosis. The hippocampus is compressed by the back of the brain. After dehydration, the hippocampus is removed. The blood supply to the posterior cerebral artery is restored. However, after several times of sputum formation and relief, the posterior cerebral artery was damaged by hypoxia, resulting in hemorrhagic softening on the inside of one side of the occipital lobe. This change is a large piece of hemorrhagic, not exactly the same as the normal hemorrhagic softening point type. Hemorrhagic softening under the microscope is basically the same as anemia softening, but there is only one type of hemorrhagic lesion of different sizes. After a long time, it can be seen that the lattice cells contain hemosiderin. Therefore, in the late stage of the lesion, although a small number of hemosiderin-containing lattice cells can be seen in the recovery period, if a yellow cyst wall or a yellow liquid is encountered during the general examination, it can be presumed to be a hemorrhagic softening result.

In patients with atherosclerosis, transient ischemic attack often occurs, which is characterized by transient single-limb or hemiparesis, limb sensory disturbance or aphasia, and complete recovery within 24 hours. In the past, clinicians thought that it was caused by cerebral vasospasm, but the hardened arteries were not prone to paralysis, so this explanation is not acceptable. According to meticulous clinical observations, combined with the advent of CT and the continuous exploration of autopsy work, it is now believed that this short episode, due to the temporary blockage of a small artery by a small embolism, causes dysfunction, but has not caused tissue necrosis. The embolus has fallen off. As the author had encountered a patient, the left eye suddenly became blind, and a glass-like embolus in the left axillary arteriole was found during the examination. After a few hours, the patient recovered vision and the fundus was completely normal. The other part, probably due to the formation of a small softening lesion, but far away from important structures such as the inner capsule or ascending sensory fibers, the slight edema caused by compression of these fibers disappears within a few hours, so the function is fully restored, but the softening is still present. The recent application of CT has greatly helped explain this phenomenon. If a patient has a hemiplegia in his medical history, CT may have found 3 softening lesions, indicating that the other two did not cause symptoms. Sometimes patients have never had a stroke, and CT can find 2 or 3 softening lesions. The autopsy workers actually noticed that some patients died as a result of a stroke, but two other old softening lesions were found in the brain. Explain that the lesions in these quiet areas, if close to important structures, may cause a brief episode of the patient due to edema, which proves that many so-called transient ischemic attacks are not without pathological basis. Another so-called reversible ischemic nervous system dysfunction, which is a neurological dysfunction such as monotherapy, sensory disturbance, aphasia, etc., completely recovered within 3 weeks. The symptoms are caused by softening close to important structures. The author encountered a patient with sudden left hemiplegia and complete recovery in 3 weeks, but CT found a softening lesion in the right nucleus, which further indicates that the so-called transient reversible cases are actually caused by softening lesions, and their pathology. basis. As long as the clinician understands the pathogenesis, these terms can be retained and benefit the patient's psychological comfort. In 1993, Fries et al reported that the patient's internal capsules were fully recovered after softening of the hind limbs. He used magnetic resonance imaging to find that the hind limbs of the internal capsule did soften. This is another powerful indication that the brain has a complete compensatory function.

A small number of patients died due to a wide range of softening lesions within 1 day after the onset; some due to the spread of thrombus, the softening lesions expanded and died within 1-2 months; most of them were relieved by the congestion and edema of the tissue surrounding the softening lesion. The compensatory effect, the function gradually recovers; some patients may eventually recover or only have minor sequelae. Some patients suffer from softening damage to important structures, such as the internal capsule, leaving serious sequelae such as hemiplegia and sputum.

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