What Is Encephalomalacia?

The arterial supply in the brain is extremely rich, and the collateral circulation is also good. Therefore, from the anatomical point of view, any small artery in the brain is not a terminal artery. Functionally, these are indeed terminal arteries. Due to the extremely high oxygen demand of the brain tissue, once the arteries are obstructed, the softening of the supply area will inevitably lead to the infarction of the organs. Softening is divided into major softening and minor softening according to its size and which arterial blood supply category. The larger ones are lesions in the area of blood supply of the cerebral aorta, such as the internal carotid artery, mostly in the cortex and white matter of the cerebral hemisphere. Artery, such as the middle cerebral artery or vertebral-basal artery perforating branch occlusion, is mostly distributed in the optic mast, basal ganglia and the upper part of the brainstem. Some scholars call the larger the softened, the smaller the cavity, and the majority of the cavity is the cavity. status. There are many reasons for softening and cavity state.

Brain softening

Due to the extremely high oxygen demand of the brain tissue, once the arteries are obstructed, it will inevitably lead to the softening of the supply area, which is the infarction of other organs. The larger one is softened and the smaller one is cavity. Most cavity is called cavity state. Causes of softening and lacunar states are embolism, arterial thrombosis, arterial spasm, and circulatory insufficiency. Softening can be divided into two types: anemia and hemorrhage. Arterial occlusion can cause anemia softening or hemorrhagic softening. Vein occlusion is almost completely hemorrhagic softening. The pathological process of anemia softening can be divided into three phases: necrotic phase, softening phase and repair phase. Cells in the softened area have been necrotic, cells in the ischemic penumbra (semi-lunar zone) are apoptotic or pre-apoptotic, with low function, and neurological and motor system dysfunction may occur.

Causes of cerebral softening disease

Cerebral embolism

In the past, softening was thought to be caused by thrombosis. In recent years, many parties have proved that most of the softening is at least 50% -60% due to embolism. The source of emboli is mostly mural thrombus in the heart, neoplasms or intracardiac myxomas, and atherosclerotic plaques that fall off from the aorta. Occasionally, it can also be tumor emboli of malignant tumors and fat emboli in fractures.

Cerebral softening arterial thrombosis

The causes include the various arterial lesions described in the previous section. The most common are atherosclerosis, followed by various arteritis. In addition to blocking the arteries to form thrombus, atherosclerotic plaques can also fall off and cause embolism.

Cerebral arterial spasm

Normal arteries are less prone to spasms, and atherosclerotic arteries are less prone to spasms. It is confirmed by angiography that primary subarachnoid hemorrhage, meningitis, and angiography itself can cause cerebral vasospasm, and then cause insufficient blood supply or softening of the brain. The spasm can be caused by the stimulation of blood decomposition products or iodine.

Cerebral softening circulatory insufficiency

Common in various types of shock. Such as

Low-volume shock due to blood loss or water loss;

Cardiogenic shock due to decreased blood output due to acute heart failure;

Septic shock. Sometimes due to autonomic nerve degeneration or dysfunction, transient postural hypotension can also occur. This hypotensive state is not harmful to those with normal cerebral arteries, but if a certain cerebral artery causes softening in the blood supply range of that artery. Sometimes the degree of hypotension is severe and lasts a long time. Even if the cerebral arteries are normal, softening can occur at the junction between the middle cerebral artery and the anterior cerebral artery or between the middle artery and the posterior cerebral artery. This is called the junction softening. Another form of circulatory insufficiency is steal syndrome. If the proximal left subclavian artery is blocked before the vertebral artery is sent out, the upper limb will have blood flow from the vertebral artery during vigorous exercise to increase blood flow Reverse flow into the distal subclavian artery caused symptoms of ischemia in the vertebral-basal artery blood supply range.

Brain softening pathological changes

Softening can be divided into anemia and hemorrhagic. Arterial occlusion usually causes anemia softening, and it can also be hemorrhagic softening. Vein occlusion is almost completely hemorrhagic softening. The pathological process of anemia softening can be roughly divided into three phases: necrotic phase, softening phase, and repair phase.

Cerebral softening and necrosis

Observation from the surface of the brain is not easy to distinguish from normal, the necrotic part may be slightly swollen, and the meningeal blood vessels are highly congested. The section is slightly raised and may be slightly harder than normal.

Softening of the brain

After a few days, the lesions became significantly softer, the cut surface was pale yellow, and the boundary between gray matter and white matter was unclear.

Cerebral softening recovery

The diseased area is often sunken. The larger one is often cyst-like. The cyst wall may be smooth and contain clear or cloudy liquids. It may also be formed by a fibrous cyst bundle of various lengths and thicknesses. The smaller one is cavity-shaped. The smaller may be harder scar tissue.

Observation under the microscope: The author s subtle observations are quite different from those described in previous books. I will describe them under the microscope to observe the different performances of 30 fresh anemia softening in four weeks. Eosinophil Ischemic neurons completely disappeared on the 16th day; pale neurons-pale plasma with fewer nuclei still visible-the so-called ghost cells in the past-appeared from the 2nd day to the 19th day Can be seen; necrotic glial oligodendritic cells appeared from the first day to 15 days; myelin sheath and axonal degeneration were visible from day 1 to 27; neutral Nucleated white blood cells can be seen on the first day, and disappear on the 6th or 7th day. Lattice cells began to appear from day 5 and gradually increased to day 27; hemosiderin remained from day 8 to day 19; newly generated blood vessels started from day 4-5 to day 27. Have. From the above information, the new necrotic period should be 4 weeks, not 1-2d. The so-called second softening period is replaced by lattice cells and astrocytes and fibers at the edges. The third stage of recovery is mainly composed of astrocytes and fibers. At this time, the lattice cells have been greatly reduced. Only a few are occasionally between the glial fibers, and some may contain hemosiderin. The ratio of astrocytes to fibers often depends on the time. The longer the time, the more fibers, the fewer cells, and the formation of atypical glial changes. Followed by ordinary connective tissue and blood vessels from blood vessels, in addition to participating in the formation of scars and capsular walls, often form the atrial septum in the capsule. Sometimes when there is no cyst on a gross examination, a small gap can be seen under the microscope. The first layer (molecular layer) of the cortex is often not damaged, only astrocytes proliferate, and the complete first layer juxtaposed with the following softened shape of the cortex and the following two or three layers are inlaid. The reason why the molecular layer is not damaged is that this layer is not supplied by each cerebral aorta, but by the meningeal artery, so it is well preserved.

The above is anemia softening. When the spot-shaped bleeding in the peripheral blood vessels of the lesion area increases, a larger bleeding focus can be formed, which is more common in gray matter. Most scholars believe that hemorrhagic softening is usually caused by embolism. Due to the sudden occurrence of softening, peripheral blood vessels can easily flow blood outside the damaged blood vessels. Another formation mechanism was proposed by Adam. The emboli entered the artery and blocked the artery. Soon, the artery was relaxed due to hypoxia, and the emboli was rushed to the distal end by blood flow. Damage and softening of surrounding tissues, causing large areas of bleeding. This results in a hemorrhagic softening and a small anemia softening in the middle, which prevents bleeding by the emboli entering the distal artery. This type is very reasonable in theory but very rare in practice. The author has not seen a typical case of this type of lesion for 40 years. This confirms that most of the hemorrhagic softening is caused by embolism, while thrombosis is rare. Another type of arterial hemorrhagic softening is caused by intermittent arterial obstruction. For example, a hemisphere of one side of the brain swells at the cerebellar notch and a hippocampal hernia is compressed. After dehydration, the hippocampus is eliminated. Blood flow to the posterior cerebral arteries resumed. But after several times of hernia formation and remission, the posterior cerebral artery was damaged by hypoxia, which caused hemorrhagic softening of the inner side of the occipital lobe. This change is massive hemorrhagic, which is not exactly the same as the ordinary hemorrhagic softening point type. Hemorrhagic softening under the microscope is basically the same as anemia softening, except that there is one more type of bleeding lesion. Over time, it can be seen that the lattice cells contain hemosiderin. Therefore, in the late stage of the lesion, a small number of hematogen-containing lattice cells can be seen even in the recovery period. Therefore, if a yellow capsule wall or a yellow liquid is encountered during a general examination, it can be presumed to be a hemorrhagic softening outcome.

Relationship between cerebral softening lesions and clinical

Patients with atherosclerosis often have transient ischemic attacks, which are manifested as transient uniplegia or hemiplegia, limb dysfunction, or aphasia, and they fully recover within 24 hours. In the past, clinicians thought that it was caused by cerebral vasospasm, but the hardened arteries were less prone to spasm, so this explanation is no longer acceptable. Based on meticulous clinical observation, coupled with the advent of CT and the continuous exploration of autopsy work, it is now believed that this short-term attack was caused in part by a small embolus temporarily blocking a small artery, causing dysfunction, but not yet causing tissue necrosis. The emboli has come off. Just as the author had encountered a patient who suddenly lost his vision in the left eye, he found a vitreous emboli in the small arteries of the left fundus. After a few hours, the patient recovered vision and the fundus was completely normal. On the other hand, it may be due to the formation of small softening foci, but it is far away from important structures such as the inner capsule or ascending sensory fibers. The slight edema caused by pressing these fibers disappears within a few hours, so the function is completely restored, but the softened foci still exist. The recent application of CT has greatly helped explain this phenomenon. If a patient has a hemiplegia in his medical history, CT may detect three softening lesions, indicating that the other two did not cause symptoms. Sometimes patients have never had a stroke, and CT can detect 2 or 3 softening lesions. The autopsy worker actually noticed that some patients died of a stroke, but two other old softening lesions could be found in the brain. It shows that if these lesions in the quiet area are close to important structures, they may cause transient attacks due to edema, which proves that many so-called transient ischemic attacks are not without pathological basis. Another type of so-called reversible ischemic nervous system dysfunction, which involves neurological dysfunction such as monoplegia, sensory disturbance, aphasia, etc., is fully recovered within 3 weeks. Symptoms are caused by softening near important structures. The author encountered a patient who suddenly developed left hemiplegia and recovered completely in 3 weeks, but CT found a softened focus on the right putamen, which further illustrates that the so-called transient reversible cases are actually caused by softened focus and have 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 capsular hind limbs were softened and still fully recovered. He used magnetic resonance examination to find that the hind limbs of the inner capsule were indeed softened. This is a strong indication that the brain has a complete compensation function.

A small number of patients died within 1 day after the onset of disease due to a wide range of softening lesions; some died within 1-2 months due to the spread of thrombus and expansion of the softened lesions; most of the symptoms were relieved due to the congestion of the tissues surrounding the softened lesions and the disappearance of edema. Compensatory effect, gradually recovering function; some patients may basically recover or have only minor sequelae. Some patients damage important structures due to softening, such as the inner capsule, but they have severe sequelae such as hemiplegia and monoplegia.

Cerebral softening prevention and care

Eat more celery, apples, fish protein, drink more water, eat less high-fat, high-cholesterol foods, do not abuse drugs, do not smoke, do not drink too much, and live a regular and reasonable diet;

Get enough sleep on time; exercise properly; learn to adjust your emotions, treat stress, open your mind, and cultivate a variety of hobbies. ^[1]