large cerebral venous aneurysm

Introduction

Introduction to large cerebral cerebral tumor The cerebral large venous tumor is mainly a tumor-like dilatation of the great cerebral vein rather than a true aneurysm, so it is also called a large venous aneurysmal vascular malformation. This disease is a relatively rare cerebrovascular malformation. basic knowledge The proportion of illness: 0.004% Susceptible people: no specific people Mode of infection: non-infectious Complications: pulmonary hypertension hydrocephalus

Cause

Causes of large brain cerebral tumor

(1) Causes of the disease

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 part is degraded and eventually disappears. During the 6th to 11th week of embryonic development, if the embryonic development is abnormal for some reason, the anterior part of the cerebral vein cannot be normally degenerated and occluded, and the arteriovenous fistula can be formed. This embryological change can explain the original The arteriovenous traffic of the large cerebral venous vein is directly open to the venous wall, and is mostly located in front of and below the capsule wall. The supply artery of the venous tumor can come from the choroid plexus of the midbrain, the posterior choroid plexus, the middle cerebral artery, and the superior cerebellar artery. Branches and meningeal vessels; thalamic penetrating branches can also participate in blood supply due to siphoning.

(two) pathogenesis

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, the vein wall is gray, thick and tough. Sometimes part of the thrombosis, the diameter often exceeds 3cm, the brain tissue degeneration in the lesion range, atrophy or softening.

87% of the supply artery directly into the large cerebral veins is involved in the posterior cerebral artery, 50% is simply supplied by the posterior cerebral artery, mostly unilateral, and more common on the right side, but also for the bilateral posterior cerebral artery. Others can also be used by the brain. The anterior artery, the middle cerebral artery, and the superior cerebellar artery supply blood. 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 large cerebral vein to expand significantly. This condition is generally arteriovenous malformation. Larger, the internal arteriovenous fistula of the lesion is also larger. In short, the large cerebral cerebral ventricle is a result of a long-term high-pressure arterial blood flow, which promotes a series of hemodynamic changes and leads to the arterialization of the venous wall.

2. Mechanisms The two basic mechanisms of this disease are high-pressure blood flow shock caused by arteriovenous short-circuit and occlusion of the dural sinus.

Prevention

Cerebral large venous tumor prevention

Surgery suddenly reduces the amount of blood in the venous tumor, which can cause hemodynamic disorder in the circulatory system, increase the peripheral vascular resistance, increase the cardiac afterload, leading to severe heart failure and endangering the patient's life. Therefore, a cardiac specialist should be consulted before surgery to accurately estimate systemic blood volume and cardiac function.

Complication

Cerebral large venous complication Complications pulmonary hypertension hydrocephalus

Patients with large cerebral cerebral venous venous fistula, if the formation of intracranial arteriovenous fistula, peripheral vascular resistance decreased, increased cardiac output, increased cardiac output, leading to ventricular hypertrophy, pulmonary hypertension, can cause heart failure, in addition, due to sagittal sinus and Increased pressure in the venous system affects the absorption of cerebrospinal fluid, causing the ventricles to expand and form hydrocephalus.

Symptom

Cerebral large venous tumor symptoms common symptoms calcified brain parenchyma deep hemorrhage cortical hyperplasia heart failure cardiac hypertrophy venous continuous blood flow neonatal heart failure action wall

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 shortly after birth. Preloaded heart failure occurs in almost all children. The degree of heart failure depends on the size of the fistula and the presence or absence of venous thrombosis. The skull auscultation can smell and persist. Intracranial murmur, jugular venous oxygen saturation is significantly increased, head CR, MRI can find aneurysmal lesions, angiography on the leading and lower margins of the lesion can be seen in many small supply arteries, mostly Yasargil type I, type II and Type III, the most common type III, ultrasound examination can also find continuous blood flow in the internal jugular vein, different from the normal fluctuation of blood flow, the lesion can be detected without echo shadow, blood flow is also persistent, Surgical treatment of intracranial lesions can not improve refractory heart failure, and can reduce myocardial infarction due to lower blood pressure during surgery. Children die more than heart failure. Autopsy found ventricular paraventricular softening, deep brain hemorrhage, cortical glia. Hyperplasia, infarction and calcification, subcortical vacuolization and other pathological changes, the cerebral large veins are abnormally enlarged, and connected with many small arteries. The mechanism of brain injury is mainly arterial blood stealing. Secondary to heart failure, cerebral ischemia, hemorrhagic infarction, disease and oppression surgical trauma.

2. Infant group Clinically divided into two groups:

(1) Cardiac decompensation occurred in the neonatal period, but after treatment relief or self-remission, subsequent head circumference increased from 1 to 12 months after birth, intracranial murmur, and auscultation was evident in the posterolateral side of the head.

(2) There is no history of decompensation of the heart, the baby is seen because of the increase in head circumference, and hydrocephalus is found. The chest can be found to have cardiac hypertrophy.

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 venous vessels compressed the midbrain aqueduct, causing obstructive hydrocephalus, but in recent years, pathophysiological studies and imaging studies Studies have shown that the child's water conduit is often kept open, and the child has no clinical manifestations of hydrocephalus. There is no paraventricular edema on CT or MRI. It is believed that the pressure in the sagittal sinus and venous system is increased, affecting the absorption of cerebrospinal fluid is ventricular enlargement. The main reason is that cerebral angiography can usually show filling cystic lesions, and can dynamically observe the contrast agent into the sac, forming turbulence, occasionally, thrombosis in the lesion, completely occluding the cyst, can not be developed, such as the wall Thrombosis, the presence of the cystic cavity, can show a "target sign" on the CT. Usually, the fistula is smaller than the neonatal group, and most of them have only one fistula, which is equivalent to the Yasargil type I.

Epilepsy is also the main clinical manifestation of this group of children. Long-term brain stealing can cause cerebral ischemia, cerebral infarction and degeneration are the pathological basis of epilepsy.

3. Children in the children group over 2 years old mostly increase the incidence of head circumference, some patients may have subarachnoid hemorrhage, the heart may also have a slight enlargement, the skull auscultation can be heard and intracranial murmur, but need to be with the child's intracranial Physiological murmurs are identified, usually in normal babies or children, and can also be heard in the skull or eyeballs, with obvious ocular or temporal side, systolic murmur, and carotid murmur can disappear, but the brain has large venous murmur. It is obvious in the vicinity of the apical nodules and the posterior midline. In newborns and infants, the murmur is strong, systolic and diastolic can be heard, and it can be continuous.

4. Adult group includes older children, adolescents or young people, with a variety of clinical manifestations: subarachnoid hemorrhage, pineal body area 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.

Examine

Examination of large cerebral cerebral tumors

1. Skull X-ray film In the infant group, occasional lesion vascular calcification, in addition to the intracranial pressure increase in children, the common intracranial calcification plaque, which is a complete or incomplete ring shape of the pineal region with a diameter of 2.5 cm or more. Calcification.

2. Cerebral angiography For the 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; preferably digital subtraction of whole brain selective blood vessels Contrast, the brain shows large venous tumors more clearly, "stealing blood" arteries and reflux veins are more clear.

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 large cerebral cerebral tumor was different among the three groups. The neonatal blood supply artery could be The anterior superior direct communication of venous tumors can come from bilateral anterior cerebral arteries, bean vein arteries, thalamic penetrating arteries, anterior and posterior choroidal arteries, and sometimes the upper cerebellar arteries are also involved in blood supply. Venous tumors are generally medium in size and return blood is straight. Sinus and other sinus, 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 one or both sides of the posterior choroidal artery or brain Arterial blood supply; in the adult group, there is often a small cerebral vascular malformation in front of the venous tumor. The blood supply artery can be 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 symmetrical ventricle enlargement above the third ventricle; secondary lesions may have irregularly shaped uneven density in front of them. High and low density shadows, enhanced scanning visible and circular high density phase, continuous until the enhanced image of the skull, suggesting 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. The boundary is clear, especially the sagittal position. Not only the tumor sac, but also the straight sinus of drainage can be seen. 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 intralesional blood. The flow pattern provides a non-invasive means for the screening of lesions. For the accompanying general conditions such as cardiopulmonary function, brain function evaluation can be performed by arterial blood gas analysis, chest X-ray, EEG, electrocardiogram, renal function, blood electrolyte examination.

Diagnosis

Diagnosis and diagnosis of large cerebral cerebral tumor

Diagnostic criteria

The diagnosis of this disease mainly depends on the age of onset and clinical manifestations, but the diagnosis requires radiological examination, neonatal refractory heart failure with intracranial vascular murmur; infants with hydrocephalus should consider the possibility of this disease, for can hear Intracranial vascular murmur or subarachnoid hemorrhage, the diagnosis can be basically determined, further diagnosis of feasible cerebral angiography, CT scan or MRI.

Differential diagnosis

Large cerebral venous enlargement is also seen in other conditions or lesions, and should be recognized 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. The treatment of these two lesions should treat the primary lesion instead of the large vein itself.

2. Large varicose veins of the brain belong to normal variation, without accompanying arteriovenous short circuit.

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