cortical gliosis
Introduction
Introduction Cortical gliosis, infarction and calcification, subcortical vacuolization and other pathological changes, abnormal cerebral large veins, and connected with many small arteries. The mechanism of brain injury is mainly arterial stealing, cerebral ischemia secondary to heart failure, hemorrhagic infarction, lesion compression and surgical trauma.
Cause
Cause
The large cerebral vein originates from the venous return system of the intermediate structure of the drainage choroid plexus. At first, the vein does not communicate with the deep intracerebral vein. About 11 weeks after the embryonic development, the posterior part of the vein communicates with the internal cerebral vein to form the great cerebral vein and the vein. The Ministry degenerates and eventually disappears. During the 6th to 11th week of embryonic development, if the embryonic development is abnormal due to some reason, the anterior portion of the cerebral vein cannot be normally degenerated and occluded, and arteriovenous fistula can be formed.
This embryological change can explain that the arteriovenous traffic of the primary cerebral vein is directly open to the venous wall and is mostly located in front of and below the wall. The supply arteries of venous tumors may come from the cerebral plexus plexus, the posterior choroid plexus, the middle cerebral artery, the branch of the superior cerebellar artery, and the meningeal blood vessels; the thalamic penetrating branch may also participate in blood supply due to siphoning.
1. Pathology: The main pathological change of this disease is a short circuit between the cerebral artery and the great cerebral vein. A large amount of arterial blood directly enters the great cerebral vein, making it extremely dilated, round or oval, and the vein wall is gray and thick. Tough; sometimes partial thrombosis, often more than 3cm in diameter. Brain tissue degeneration, atrophy or softening within the lesion. 87% of the supply artery directly into the large cerebral veins is involved in the posterior cerebral artery, and 50% is simply supplied by the posterior cerebral artery. It is mostly unilateral, and is more common on the right side. It can also supply blood to the bilateral posterior cerebral artery. Others can also be supplied by the anterior cerebral artery, the middle cerebral artery, and the superior cerebellar artery. Most of the patients belong to the above situation, but in some cases, the drainage vein of the cerebral arteriovenous malformation is introduced into the great cerebral vein, which causes the great cerebral vein to expand significantly. In this case, the arteriovenous malformation is large, and the arteriovenous fistula is also large. In short, large cerebral cerebral venous tumors are caused by long-term high-pressure arterial blood flow, which triggers a series of hemodynamic changes leading to the arterialization of the venous wall.
2. Mechanism: The two basic mechanisms of this disease are high-pressure blood flow shock caused by arteriovenous short circuit and occlusion of dural sinus.
Examine
an examination
Related inspection
Brain Doppler Ultrasound (TCD)
Symptoms and signs
Large cerebral cerebral anatomy, according to the age of onset can be divided into four age groups:
1. Neonatal group: The typical manifestation is high-output, preloaded heart failure shortly after birth, which occurs in almost all cases.
The extent of heart failure depends on the size of the fistula and the presence or absence of venous thrombosis. Skull auscultation can smell and continue intracranial murmur. Jugular venous oxygen saturation was significantly increased. Aneurysmal lesions can be found in the CR and MRI of the skull. Many small supply arteries can be seen on the leading and lower edges of the angiography. Most of them belong to Yasargil type I, type II and type III, and most of them are type III. Ultrasound examination also found continuous blood flow in the internal jugular vein, which is different from normal volatility. There is no echogenic shadow at the lesion, and the blood flow is also persistent. Surgical treatment of intracranial lesions does not improve refractory heart failure, and may induce myocardial infarction due to decreased intraoperative blood pressure. The child died of heart failure. At autopsy, there were pathological changes such as ventricular paraventricular softening, deep brain parenchymal hemorrhage, cortical gliosis, infarction and calcification, and subcortical vacuolization. The cerebral large veins were abnormally enlarged and connected with many small arteries. The mechanism of brain injury is mainly arterial stealing, cerebral ischemia secondary to heart failure, hemorrhagic infarction, lesion compression and surgical trauma.
2. The infant group is clinically divided into two groups:
(1) Cardiac decompensation occurred in the neonatal period, but it was relieved by treatment or relieved by itself. Subsequently (1 to 12 months after birth), the head circumference increased, intracranial murmur, and the auscultation of the posterolateral side of the head was obvious.
(2) There is no history of cardiac decompensation. The baby was seen with an enlarged head circumference and found hydrocephalus. The chest radiograph can be found in the heart.
The ventricles of the children can be significantly enlarged, involving the lateral ventricle and the third ventricle. In the past, the reason for the enlargement of the ventricle was that the enlarged large cerebral veins pressed the midbrain aqueduct and caused obstructive hydrocephalus. However, in recent years, pathophysiological studies and imaging studies have shown that the children's water conduits are often kept open, and the children have no clinical manifestations of hydrocephalus. There is no paraventricular edema on CT or MRI. It is currently believed that the increase in pressure in the sagittal sinus and venous system affects the absorption of cerebrospinal fluid is the main cause of ventricular enlargement. Usually, cerebral angiography can show a filling cystic lesion, and can dynamically observe the contrast agent into the capsule to form turbulence. Occasionally, thrombosis occurs in the lesion, completely occluding the cyst and cannot be developed. If a thrombus is formed on the wall of the capsule, the cystic cavity is present and a "target sign" can be displayed on the CT. Usually, this type of mouth is smaller than the newborn group, and most of them have only one mouth, which is equivalent to the Yasargil type I. Epilepsy is also the main clinical manifestation of this group of children. Stealing blood in the brain for a long time can cause cerebral ischemia. Cerebral infarction and degenerative changes are the pathological basis of epilepsy.
3. Children's group: Most children over the age of 2 have increased their head circumference.
Some patients may have subarachnoid hemorrhage and the heart may be slightly enlarged. Skull auscultation can be heard and intracranial murmur. However, it needs to be differentiated from the intracranial physiological noise of children. Generally, in normal infants or children, it is also possible to smell murmurs in the skull or the eyeball, and the eyeball or the temporal side is obvious, the systolic murmur is increased, and the compression of the carotid artery murmur can disappear. However, the cerebral venous murmur is obvious in the vicinity of the apical nodules and the posterior midline. In newborns and infants, the murmur is strong, and both systolic and diastolic can be heard, and it can be continuous.
4. Adult group: including older children, adolescents or youth. A variety of clinical manifestations: subarachnoid hemorrhage, pineal body occupying, high intracranial pressure and hydrocephalus. Head CT or MRI can be used for differential diagnosis. Pathophysiologically, the patient has a small arteriovenous fistula, a low flow rate, or a secondary cerebral large cerebral tumor.
Laboratory examination: no special performance.
Other auxiliary inspections:
1. In the infant X-ray plain film group, occasional lesion vascular calcification, in addition to the increase of intracranial pressure in children, the common intracranial calcification. It is a complete or incomplete annular calcification with a diameter of 2.5 cm or more in the pineal region.
2. Cerebral angiography is the main means of diagnosis of large cerebral venous tumors. At least 3 selective cerebral angiography should be performed, including bilateral internal carotid artery and one side vertebral artery angiography; it is best to perform digital subtraction whole brain selective angiography to make the brain large venous tumor show more clearly, "stealing blood" Arteries and reflux veins are more defined. The cerebral angiography showed that the large cerebral veins expanded ovally, and the diameter was generally 4 to 5 cm. The straight sinus also expanded significantly. The blood supply artery of the great cerebral cerebral tumor differed among the three groups of patients. The neonatal blood supply artery can be directly transported in front of the venous tumor, which can come from the bilateral anterior cerebral artery, the bean vein artery, the thalamic penetrating artery, the choroidal anterior and posterior arteries, and sometimes the upper cerebellar artery participates in blood supply. Venous tumors are generally medium in size, with returning blood flowing into the straight sinus and other sinuses. The feeding artery of the infant group is often located on the lower lateral side of the venous tumor, and is supplied by the posterior choroidal artery. In the child group, the blood supply artery is often located in front of or above the venous tumor, and is supplied by one or both of the posterior choroidal artery or the anterior cerebral artery; There is often a small cerebrovascular malformation in front of the venous tumor. The blood supply artery can come from the posterior choroidal artery and the thalamic penetrating artery, and the blood is introduced into the great venous system of the brain. Understanding the drainage vein is important for judging the prognosis.
3. CT scan shows a well-defined oval high-density image of the pineal region, often accompanied by a symmetric ventricle enlargement above the third ventricle; secondary lesions may have irregularly shaped uneven density in front of them. High and low density shadow. Intensive scanning can be seen with a circular high-density phase, continuous until the enhanced image of the skull, suggesting a straight sinus expansion.
4. MRI of the great cerebral venous tumor of MRI is very typical. It is a circular no-signal area, which is caused by blood flow and empty effect. Its boundary is clear, especially sagittal, not only the tumor sac, but also the straight sinus of drainage. The brain sinus and so on.
5. Other MR angiography and Doppler ultrasonography are effective adjuvants for the diagnosis of large cerebral cerebral tumors. Especially for children with patent forcing, Doppler ultrasound can determine intracranial hemodynamic changes and blood flow patterns in the lesions, providing a non-invasive means for screening lesions. For the accompanying general conditions such as cardiopulmonary function and brain function evaluation, arterial blood gas analysis, chest X-ray, EEG, electrocardiogram, renal function, blood electrolyte examination, and the like can be used.
Diagnosis
Differential diagnosis
Large cerebral venous enlargement is also seen in other conditions or lesions, and attention should be paid to identification. Because they are different in treatment from the primary cerebral large cerebral tumor.
1. Large cerebral venous enlargement is seen in the secondary cerebral venous tumor caused by brain AVM, or the large cerebral vein compensation caused by dura mater AVF. Treatment of these two lesions should treat the primary lesion, not the large vein itself.
2. Large varicose veins of the brain belong to normal variation, without accompanying arteriovenous short circuit.
