Arteriovenous malformations of the vein of Galen. Venous drainage from the brain

- a group of anomalies in the development of the great cerebral vein, resulting from the persistence of embryonic vessels with the formation of arteriovenous shunting. Manifested by heart failure, hydrocephalus, lag in physical and mental development. Neurological symptoms are characteristic, aneurysm rupture with intracranial hemorrhage is possible. Diagnosis of an aneurysm of the vein of Galen is carried out during prenatal ultrasound screening with Doppler ultrasound. In newborns, the diagnosis is confirmed by CT, MRI, angiography. The treatment is surgical, embolization of the vessels supplying the vein is carried out.

Classification and symptoms of an aneurysm of the vein of Galen

Arteriovenous malformation is located in the anterior cranial fossa, above and behind the visual tubercles, in the so-called cistern of the vein of Galen. Structurally, there are three types of aneurysm of the vein of Galen. The intramural form is characterized by the opening of the arterial trunk directly into the great cerebral vein. In the choroidal form of the vascular anomaly, arteriovenous shunts are located in the choroidal fissure and flow into either a large vein or pathological embryonic veins. The parenchymal form of an aneurysm of the vein of Galen is distinguished by the location of numerous shunts in the brain parenchyma.

Pathology is manifested from birth in 50% of patients. The leading symptom is heart failure, which develops as a result of a high venous return of blood from the brain and, accordingly, an increasing load on the left side of the heart. Since the aneurysm of the vein of Galen is still formed in utero, by birth, heart failure has a high risk of decompensation. Clinically, this is expressed in fatigue during feeding, generalized edema, shortness of breath due to interstitial pulmonary edema. In the future, heart failure becomes one of the reasons for the lag in physical development.

Hydrocephalus is an unfavorable prognostic sign, since it indicates occlusion of the Sylvian aqueduct or a significant volume of blood discharge into the venous bed. The child's head has been enlarged since birth, dilated veins are visible on its surface. There may be vomiting, exophthalmos, focal neurological symptoms in the form of ptosis, strabismus. Increased intracranial pressure is sometimes accompanied by convulsions. In the future, a mental retardation is characteristic, which is also associated with insufficient nutrition of the brain tissues. Less commonly, an aneurysm of the vein of Galen is manifested by symptoms of intracranial hemorrhage: loss of consciousness, convulsions, etc.

Diagnosis of an aneurysm of the vein of Galen

Primary diagnosis becomes possible with routine ultrasound screening in III trimester pregnancy. An aneurysm of the vein of Galen is visualized as an anechoic mass in the center of the head. Color Doppler imaging is used for confirmation. The method is different a high degree reliability. In the absence of prenatal diagnosis, establishing the presence of a vascular anomaly after childbirth can be problematic. Firstly, the disease is extremely rare, therefore it becomes an exception for the pediatrician among many other causes of heart failure and hydrocephalus. Secondly, an aneurysm of the vein of Galen is not always clinically evident from the moment of birth.

Computed tomography and MRI are also widely used in diagnostic purposes. In the pictures, pathological tangles of embryonic vessels can be visualized. For further planning of treatment tactics, it is necessary to conduct angiography, which allows you to establish topographic relationships with normal vessels and detect other possible vascular anomalies. Thrombosis can be suspected by the results of angiography, therefore, contrast x-ray examination vessels remains the main one in the diagnosis of aneurysm of the vein of Galen. Exactly this method allows vascular surgeons to plan the tactics of surgical intervention.

Treatment, prognosis and prevention of aneurysm of the vein of Galen

Currently, endovascular embolization of the vessels supplying the aneurysm remains the main method of therapy. The recommended age of the child for the operation is 2-6 months. At the stage of preoperative preparation, anticoagulants are used to prevent vascular thrombosis, as well as cardiotonic drugs to compensate for heart failure. If there are signs of severe hydrocephalus, a shunt is indicated to normalize intracranial pressure. A ventriculoperitoneal shunt is usually performed. open surgical operations in the treatment of aneurysm of the vein of Galen are practically not used.

The prognosis of the disease is often unfavorable. Development modern methods neurosurgery has reduced mortality to 50-70%. Nevertheless, children who survived after the operation are mentally retarded, and neurological symptoms persist. Primary prevention performed prenatally. When an aneurysm of the vein of Galen is detected on ultrasound, doctors and parents determine the tactics of further pregnancy management. Most experts recommend operative delivery by caesarean section followed by the therapy described above. Currently, the mortality in such cases reaches 80%.

special kind arteriovenous malformations, characteristic mainly for the pediatric group of patients.

Vienna Galena (vena magna cerebri) is one of the main venous collectors of the brain, which collects blood from its internal structures(basal nuclei, visual tubercles, transparent septum, choroid plexuses of the lateral ventricles of the brain) and flows into the direct sinus. By modern ideas, arteriovenous malformations (AVM) of the vein of Galen is a congenital malformation of the cerebral vessels associated with a delay in the reverse development of arteriovenous communications that exist in the embryonic period of development, with the obligatory presence of an aneurysmally dilated vein of Galen. Despite the fact that AVMs of the vein of Galen are very rare (1% of all intracranial vascular malformations), this anomaly is diagnosed in one third of cases of AVMs in the neonatal and early childhood period. In boys, it occurs 2 times more often.

This malformation is characterized by hypoplasia of the muscle and elastic fibers of the middle layer. big vein brain, in connection with which even slight increase venous pressure can lead to diffuse or limited varicose veins that gradually progress. There are diffuse and saccular dilatations of the vein of Galen. According to the classification of A. Berenstein and P. Lasjaunias (1992), based on angiostructural differences, there are two types of AVMs of the vein of Galen:

    Type 1 - mural: a fistulous structure is characteristic, in which the afferent arteries approach the wall of the enlarged large cerebral vein and directly open into the lumen of the latter;
    Type 2 - choroidal: characterized by the presence of a pathological vasculature supplying cerebral AVMs or dural arteriovenous fistulas draining into the true but dilated vein of Galen.


A significant increase in the size of the Galen vein causes mechanical pressure on the surrounding structures of the brain, causing their atrophy, dislocation, impaired venous outflow and liquorodynamics, and ultimately progressive hydrocephalus of the ventricular system of the brain. The manifestation of the disease occurs in the early childhood(extremely rare - in adults) and can be represented by hypertensive-hydrocephalic syndrome (developing as a result of occlusion of the water pipe), intracranial hemorrhage, epileptic seizures, psychomotor retardation, focal neurological symptoms, heart failure (AVM of the vein of Galen is often combined with malformations of the heart and vascular system: insufficiency of the tricuspid valve, non-closure of the foramen ovale, coarctation of the aorta). Most authors distinguish 3 types of clinical manifestations of the AVM of the vein of Galen:
    Type 1 - severe, often leading to death - cardiovascular and pulmonary insufficiency, hepatomegaly, non-communicating hydrocephalus, intracranial pulsatile noises;
    type 2 - local arterial phenomenon with the classic "steal" syndrome and underdevelopment of brain structures with severe focal disorders;
    Type 3 - local venous manifestations in the form of impaired venous outflow, increased venous pressure and CSF circulation disorders with the development of communicating hydrocephalus.
Prenatal diagnosis of AVMs of the vein of Galen using ultrasonography (ultrasound) and MRI of the fetus makes it possible to establish a diagnosis in the third trimester of pregnancy. Based on these data, it is possible to assess the size of the AVM, the presence of hydrocephalus and concomitant heart failure in the fetus, as well as adequately plan delivery and further treatment of the child (angiography is also used in children: superselective angiography, vertebral angiography, etc.). At the present stage of development of vascular neurosurgery, the method of choice in the treatment of AVMs of the vein of Galen is endovascular exclusion of the AVM: the endovascular method is the main, highly effective and low-traumatic method of treatment, with low level disability and mortality. The presence of progressive hydrocephalus with corresponding symptoms is an indication for CSF shunting before endovascular treatment. The method of choice is the imposition of a ventriculo-peritoneal shunt. In view of the rare occurrence of pathology, complex angioarchitectonics, and the peculiarities of perioperative management of patients, endovascular interventions should be performed in large federal centers of the country that have the appropriate equipment and sufficient experience in intravascular neurovascular interventions.

The goal of endovascular treatment is to minimize or stop inflow arterial blood into the venous system of the brain. At the same time, even incomplete shutdown of blood flow in the AVM in the overwhelming majority of cases leads to regression or stabilization of clinical symptoms. Optimal age patients for endovascular interventions - 3 - 5 months. However, with increasing symptoms of cardiovascular insufficiency, intervention should be carried out in more early dates. Expectant management in asymptomatic AVMs of the vein of Galen is unreasonable, since successful endovascular treatment in the first year of life, before the appearance of irreversible neurological disorders, can achieve good results. clinical results. Endovascular treatment of AVMs of the vein of Galen in older children age group and in adults are associated with a high risk of intracranial hemorrhage due to the possibility of developing hyperperfusion changes in cerebral hemodynamics due to the duration of AVM functioning.

An aneurysm of the vein of Galen is a disease that is characterized by abnormalities in the development of the vein of Galen (a vessel located in the human brain). Also, such vessels can be intertwined or have processes that come out of the vein. The disease can progress in the embryonic period, so it is associated with congenital ailments. Vessel weaves usually have strange sheaths that ordinary person thick, and in people with pathology - thin. Doctors very rarely encounter such a disease as an aneurysm of the vein of Galen.

These weaves are not supplied with blood, it goes into the veins, so the blood circulation becomes different from healthy. It is because of the low blood supply that various disorders of the brain and the appearance of the pathology of the vein of Galen occur. It is very important to remember that an aneurysm is very dangerous, because at any moment the vessels can burst and hemorrhage can form. Therefore, it is necessary to immediately consult a doctor in order not to bring the disease to a fatal outcome.

Of course, doctors still cannot find all the causes of this disease, but there are some factors that affect the development:

  • if a person has congenital damage to the vessels of the brain due to the fact that they are tortuous, bent, then this can be the cause (especially hereditary predisposition);
  • if a person has high pressure, then it presses on the already damaged areas of the vessels, which leads to their rupture;
  • if a person had some kind of injury associated with damage to blood vessels or the brain, as well as various cardio - vascular diseases or a tumor, such as a brain tumor or a tumor that interferes with circulation, this can lead to aneurysms.

It is possible to identify the disease from birth only in fifty percent of patients. Since blood circulation is disturbed, sometimes there is high pressure, then there is a big load on the heart, which leads to heart failure. As already mentioned, the disease is formed in the baby even in the womb of the mother, so the signs of insufficiency are visible on the face.

From an early age, a child may show:

  • fatigue - when the mother gives the baby a breast, and the newborn gets tired when feeding;
  • edema, swollen places in certain parts body;
  • pulmonary edema.

In addition, an aneurysm of the vein of Galen can cause hydrocephalus, which is characterized by an increase in the size of the child's head, as well as pronounced veins on the scalp. In this case, symptoms such as vomiting, blurred vision, protrusion will be observed. eyeball and others. Also, due to the fact that the pressure is increased, there may be convulsions in the newborn, as well as hemorrhage.

If the mother of a newborn has noticed deviations in the behavior of her child, changes in appearance, then you should immediately consult a doctor to rule out or confirm this serious disease.

Tracking changes in the child's body is possible when examining the mother for later dates pregnancy when the fetus is fully formed. Ultrasound is often done in such a diagnosis, in which mothers are informed about the health status of their unborn child. Also, doctors sometimes do dopplerography, because it is effective in identifying such ailments.

In general, if the mother of the newborn has not been examined for the appearance of such abnormalities or they have not been identified, then it is difficult to judge pathologies when the child has already appeared.

This is due to the fact that:

  • the disease is extremely rare, therefore, its signs are not fully understood by everyone, and sometimes they are not known at all;
  • symptoms do not always appear, which delays the treatment and diagnosis of the disease.

Also, magnetic resonance imaging or CT scan, which fix changes in the vessels and detect their interweaving. For their further study, a contrast x-ray is used, which also examines the nearest vessels in order to understand the scheme of surgical intervention.

To solve problems, it is very important to have the right doctors who will explain the situation and help parents cope with this difficult matter, and it is also necessary to have diagnostic equipment that only qualified specialists have available.

Due to the fact that treatment is sometimes delayed, a person may experience a brain hemorrhage. As a result, blood enters all brain tissues, which leads to their necrosis and complete dysfunction, along with this, hydrocephalus can be detected.

Due to the gap may occur:

  • headaches, often pulsating in the brain, which are not helped by any drugs;
  • lost in space;
  • uncomfortable being in society or stress in life;
  • poor management of their actions.

Nowadays, the percentage of lives saved from this disease increases with the development of medicine and modern technologies. Most best method treatment, according to doctors, surgical intervention, which saves even the largest aneurysms.

During surgery, there is a risk of damaging the aneurysm. This is what is postoperative complications. In addition, surgical intervention goes hand in hand with traditional treatment, are issued various drugs, for example, to anesthetize the operated site or to save a person from vomiting.

Of course, despite the progress in science and medicine, doctors can not save all newborns, mortality is still very high. To save children, they are trying to identify the disease at the stage of the embryo, but this is not always possible, so now it is actively developing Technical equipment for the study of this disease.

Aneurysm of the great vein of the brain is rare vascular pathology central nervous system, accounting for about 1% of all vascular malformations of the brain.

In childhood, this pathology is much more common - about 30%.

Surgical treatment of aneurysms of the galenic vein in the recent past has been associated with big risk, and depending on the age of the patients, the lethality ranged from 30 to 90%.

With the introduction of endovascular treatment, mortality has decreased and currently ranges from 4 to 40%.

General information

Aneurysms of the vein of Galen are divided into true - primary and false - secondary. True aneurysms are spoken of in cases where arteriovenous shunting occurs directly into the galenic vein. Secondary ones include aneurysmal expansion of the galenic vein due to increased blood flow through it, while the arteriovenous shunt can be located at a distance from the galenic vein.

According to modern concepts, there are two main types of true aneurysms of the galenic vein:

1) choroidal;
2) mural.

They, in fact, are not aneurysms of the galenic vein, but represent an expansion of the embryonic, so-called median vein of the prosencephalon, located in the cistern of the velum interpositum. In the first variant - choroidal - there are multiple communications between the galenic vein, villous arteries, as well as deep perforating and terminal branches of the anterior cerebral arteries.

In the second option - mural - there are fewer sources of blood supply, they can be single and even one-sided. The choroidal type of aneurysm of the galenic vein occurs mainly in newborns and, due to the large discharge of arterial blood into the venous bed, often leads to heart failure.

Two main methods for the treatment of aneurysms of the galenic vein have been proposed:

1) straight surgical removal,
2) endovasal thrombosis.

Despite the fact that individual surgeons have demonstrated the possibility of successful excision of aneurysms of the galenic vein, at present, their endovascular occlusion is still recognized as the main method of treatment. After turning off the main sources of blood supply to the aneurysm of the galenic vein, its thrombosis occurs, followed by retraction of the clot and a decrease in the volume of the aneurysm.

However, in some cases, surgically induced or spontaneous thrombosis of the aneurysm of the galenic vein leads to occlusion of the cerebrospinal fluid at the level of the cerebral aqueduct and the posterior sections of the third ventricle, which necessitates bypass surgery or removal of the aneurysm.

Endovasal thrombosis can be carried out in different ways:

1) through the arterial bed by catheterization of the femoral artery. In this case, occlusion of the leading arteries of the aneurysm is performed;

2) retrograde along the venous bed. This can be done by puncturing the sinus drain with a catheter placed over the aneurysm, or by catheterization. femoral vein. Since 1987, the latter technique has become the main method of endovasal exclusion of aneurysms of the galenic vein.

Thrombosing of an aneurysm can also be carried out directly by puncture through the fontanel with the introduction of a thrombosing substance into the aneurysm cavity.

Direct surgical intervention for aneurysm of the vein of Galen is currently rarely used due to the high risk. As a rule, removal of an aneurysm of the great vein of the brain is carried out after endovascular or spontaneous thrombosis of the aneurysmal sac. It should be noted that spontaneous thrombosis of an aneurysm of the great vein of the brain is rare. R.W. Hurst et al described two cases and found twenty more similar observations in the literature.

The cause of spontaneous thrombosis of an aneurysm of the galenic vein is poor blood flow and obstruction of venous outflow.

Our series included three cases of thrombosed aneurysm of the galenic vein. Two of them underwent removal of the malformation.

Among them, in the first case, the aneurysm was true (Fig. 189), and in the second - false (Fig. 190). It is interesting to note that in the second case, the aneurysmal expansion of the galenic vein was combined with a large aneurysm of one of the veins of the posterior cranial fossa. In the third case, it was not possible to differentiate these two types of malformation.

Fig.189. CT (a) reveals a rounded, calcified mass located in the projection of the posterior parts of the third ventricle and the pineal region. There is a significant expansion of the ventricular system. On MRI in T1 (b) and T2 (c) modes, the mass formation has a heterogeneous structure with fairly clear CT boundaries after total excision of the aneurysm (d). The clip is superimposed on the branch of the posterior cerebral artery that supplied the aneurysm.


Fig.190. MRI in three projections shows aneurymagically dilated veins of Galen and the posterior cranial fossa on the left.

In the T1 mode, the volumetric formation has a high signal (a, b, c, d); in T2 mode - the hyperintense zone of the signal is surrounded by the hypointense zone (e, f). The malformation is clearly visualized as an isointense lesion in T1 (a) and hypointense in T2 modes (e, arrows). MR angiography using the time-of-flight technique in the arteriography (g) and vepography (h) modes, as well as the phase-contrast technique (i), did not detect blood flow through the pathological vessels, which indicated their thrombosis.

Schematic representation (j) of the aneurysmal expansion of the vein of Galen (1) and the posterior cranial fossa (2). The vascular malformation of the posterior cranial fossa on the right (3) is supplied by the right posterior inferior cerebellar artery (4). The malformation drains into the cavity of the dilated galenic vein through the lateral veins of the pons (5). Postoperative CT scans (l,m) show complete removal thrombosed aneurysm.

Clinical example

In a 9-year-old girl, the disease manifested itself 2 years before hospitalization, when, against the background of full health weakness appeared in the left arm and in the muscles of the shoulder, the girl began to drag her left leg. According to the mother, during the year before hospitalization, the child's memory decreased, left hand lagged behind in physical development.

When she entered the Institute, her condition was satisfactory, she was fully oriented in place and time. The level of mental development corresponds to age, although in physical development it lags behind. The rest of the somatic status without visible pathological abnormalities. Clinical, biochemical analyzes are also within the normal range. ECG without pathology.

Chest x-ray showed no pathology of the heart and lungs. In the neurological status, against the background of signs of stagnation in the fundus, some awkwardness of movements and a decrease in strength in the left limbs were revealed. When walking left leg"clubfoot". The finger-nose test was performed uncertainly with the left hand. Left-sided spontaneous installation nystagmus. No symptoms of midbrain involvement were identified.

At electroencephalogram (EEG) against the backdrop of expressed general changes caused by signs of dysfunction of the subcortical-diencephalic structures of the brain, a slowdown in the cortical rhythm of the spruce temporal region was detected with a high severity of epileptic signs in the right temporal region.

At computed tomography (CT) a rounded, calcified volumetric formation was determined, located in the projection of the posterior sections of the third ventricle and the pineal region with a significant expansion of the ventricular system (Fig. 189).

Vertebral and carotid angiography revealed no pathological vasculature. The great cerebral vein, as well as the internal and basal veins, were not contrasted^. The direct sinus was not visualized. The detected volumetric formation was regarded as a dermoid cyst of the pineal region. The suggestion of an aneurysm of the galenic vein, although expressed, was rejected, since there were no signs of arteriovenous shunting.

The patient was operated on using the infratentorial supracerebellar access. During the operation, a thrombosed aneurysm of the galenic vein was discovered and removed. The operation went without complications. The control CT scan showed total removal of the aneurysm.

In the second case, a 5-year-old girl developed the disease shortly after birth. According to her mother, the girl began to walk late (after 15 months), her gait was pretentious - on tiptoe. She was slow, cautious, different from other children, did not take part in games, but by the age of 4-5, all these features smoothed out, in kindergarten did not differ from peers.

3 months before hospitalization, the temperature suddenly rose to 39.5 ° C with severe headache. For a month, forced posture: "on all fours", with his head buried in the pillow. From the same time - a fixed position of the head with an inclination to the right. Parents noticed a difference in the width of the palpebral fissures - more on the left.

A CT scan revealed a large brain tumor, and the child was hospitalized at the Institute.

Upon admission, the condition is satisfactory, the development of the child corresponds to the age. Somatic status without features. At electrocardiography (ECG) only sinus tachycardia - up to 103. Blood pressure (A/D)- 100/60. Head size is normal, no meningeal signs, mental development age appropriate.

The left palpebral fissure is somewhat wider than the right, the right eyeball does not lead to the external commissure. Visual acuity of 0.5. The boundaries of the visual fields are within the normal range. Congestion in the fundus.

Performs coordination tests less deftly with the left hand. In the Romberg pose, he sways. gait with eyes closed unsure - staggers to the left. Multiple spontaneous nystagmus, optonistagmus sharply weakened to the left. Violation of statics, gait and coordination in the left hand.

CT was performed to clarify the diagnosis. Magnetic resonance imaging (MRI) in the standard and angiographic modes, which revealed a vascular malformation of a complex configuration, located in the posterior cranial fossa and the surrounding cistern (Fig. 190). Judgments about the true nature of the pathology were ambiguous, and only a comparison of the data of the examinations with the features found during the operation made it possible to get a clearer idea of ​​the nature of the vascular deformity. The finally discovered mass was regarded as a thrombosed secondary aneurysm of the galenic vein.

Arterial inflow was carried out from the right posterior lower cerebellar artery, which was connected to a large aneurysmal cavity with a diameter of about 3 cm. This aneurysmal cavity, in turn, was connected by a rather powerful duct to a giant dilated galenic vein (3.9x2.9x3.8). The latter included the end sections of the basal veins. Magnetic resonance angiography did not reveal blood flow in the malformation, which indicated its thrombosis.

Both CT and MRI showed severe brainstem compression and mild hydrocephalus. Although a thrombosed vascular malformation of the galenic vein system was suggested before the operation, there was no complete certainty in this diagnosis.

Indirect signs of a thrombosed aneurysm of the vein of Galen were the absence of contrast enhancement of the internal veins and the vein of Galen, as well as an excessive pattern of convexital veins during direct angiography (Fig. 191).


Fig.191. Angiography of a patient with a thrombosed aneurysm of the vein of Galen. venous phase. Lack of deep vein enhancement and excessive development of convexital veins.

Thrombosed vascular cavities were excised by extended trepanation of the posterior cranial fossa. First, an aneurysmal formation associated with the inferior cerebellar artery in the basal parts of the posterior cranial fossa was excised; this allowed the supracerebellar approach to widely expose and excise the vascular formation located in the pineal region, which turned out to be a sharply enlarged galenic vein filled with dense blood clots.

Morphological study showed that the walls of the excised aneurysms were formed by coarse fibrous connective tissue with areas of lymphocytic infiltration. On the surface of the basally located aneurysmal cavity, conglomerates of malformed pathological vessels were found - arteriovenous malformation.

Control CT confirmed the effectiveness of the operation. By the time of discharge, two weeks after the removal of the aneurysm, general state the child is satisfactory, with virtually no increase in neurological symptoms.

In one of our observations, a thrombosed aneurysm of the vein of Galen was found. Due to severe hydrocephalus, a bypass operation was performed. Two months after the operation, the aneurysm significantly decreased in volume, and therefore there was no need for direct intervention (Fig. 192).


Fig.192. Thrombioropic aneurysm of the vein of Galen.

CT (a, b, c) in the pineal region reveals an annular mass with a hypodense central part and severe occlusive hydrocephalus. On vertebral (d, e) and carotid angiography (f, g), the aneurysm is not contrasted!, but on vertebral angiography, a sharply dilated right posterior cerebral artery is visualized. The deep veins of the brain are not contrasted (g), which indicates a sharp reduction in blood flow through them.

CT scan 2 months (h, i) after examination and shunt placement; revealed a significant reduction in the volume of thrombosed aneurysm.

Mural aneurysms of the galenic vein are more often diagnosed in childhood and proceed more favorably. This type of aneurysm of the galenic vein should include the first of the observations described by us, since only one source of blood supply was found - one of the villous arteries.

The vascular malformation revealed in the second observation can most likely be attributed to a secondary aneurysm of the vein of Galen. In this case, the galenic vein expanded to a gigantic size due to the discharge of blood into it from the arteriovenous anastomosis, which was supplied from the posterior inferior cerebellar artery. Indirectly, the spread of a thrombus from the giant dilated galenic vein at the mouth of the basal veins also indicates the secondary expansion of the galenic vein.

Diagnostics

Diagnosis of thrombosed aneurysms of the galenic vein presents certain difficulties. In the observations we described before the operation, a thrombosed aneurysm of the galenic vein was suggested, however, the final diagnosis in both cases was made only during the operation. The main difficulty in recognizing thrombosed vascular malformations is complete absence blood flow through it.

According to CT data, typical for a thrombosed aneurysm can be considered its typical localization, correct round shape and a calcified capsule, as found in the first observation.

However, in the second observation, it was the MR characteristics of the formation that made it possible to make an assumption about a thrombosed aneurysm of the galenic vein. A typical change in the MP signal is hyperintense with a shortened T1, characteristic of methemoglobin in the central part of the neoplasm, and a hypointense signal in the form of a rim around the periphery, typical of hemosiderin deposition. The presence of a thrombosed aneurysm of the galenic vein was also indicated by the results of MP-angiography using time-of-flight and phase-contrast techniques.

In the observations described by us, aneurysms of the galenic vein were clinically manifested as volumetric formations with cerebral, local symptoms, the presence of occlusive hydrocephalus, which was the indication for their surgical removal.

A.N. Konovalov, D.I. Pitskhelauri

  1. Great cerebral [[Galena]] vein, v. magna cerebri []. A short trunk between the junction of two internal cerebral veins and the beginning of the direct sinus. Rice. A, V.
  2. Internal cerebral veins, w. internae cerebri. Each of them begins at the interventricular opening, passes in the transverse groove of the brain between the fornix and the thalamus, or in the roof of the third ventricle. Both vessels, connecting together, form a large cerebral vein. Rice. A, V.
  3. Superior villous vein, v. choroidea superior. Runs along choroid plexus lateral ventricle to the interventricular foramen and receives branches from the hippocampus, fornix and corpus callosum. Rice. A.
  4. Superior thalamostriatal vein (terminal vein), v. thalamostriata superior (v. terminalis). Passes in the groove between the thalamus and the caudate nucleus, taking branches from the structures surrounding the thalamus. At the interventricular foramen it opens into the superior villous vein. Rice. A.
  5. Anterior vein of the transparent septum, v. anterior septi pellucidi. Passes in a transparent septum and collects blood from the frontal lobe and knee of the corpus callosum. It flows into the superior thalamostriatal vein. Rice. A, V.
  6. Posterior vein of the transparent septum, v. posterior septi pellucidi. It starts from the roof of the lateral ventricle and joins the internal cerebral vein. Rice. IN.
  7. Medial vein of the vestibule of the lateral ventricle, v. medialis atrii ventriculi lateralis. Carries out the outflow of blood from the parietal and occipital lobes. Passes along the medial wall rear horn lateral stomach. Rice. A.
  8. Lateral vein of the vestibule of the lateral ventricle, v. lateralis atrii ventriculi lateralis. It starts from the occipital and temporal lobes. Passes as part of the lateral wall of the lateral ventricle in front of the posterior horn. Rice. A.
  9. Veins of the caudate nucleus, vv. nuclei caudati. Rice. A.
  10. Lateral direct veins, vv, directae laterales. They start from the wall of the lateral ventricle and flow into the internal cerebral vein. Rice. A.
  11. Posterior vein of the corpus callosum, v. posterior corporis callosi. Passes downward from the ridge of the corpus callosum. Rice. A, V.
  12. Dorsal vein of the corpus callosum, v. dorsalis corporis callosi. It wraps around the corpus callosum. Rice. IN.
  13. Veins of the brainstem, w. trunciencephali.
  14. Anterior pontine cerebral vein, v. pontomesencephalica anterior. It is a continuation of the veins of the medulla oblongata in the region of the interpeduncular fossa. Carries out the outflow of blood from the brain stem into the petrosal and basal veins. Rice. IN.
  15. Bridge veins, w.pontis. Most of them flow into the stony or anterior pontine-medium cerebral veins. Rice. IN.
  16. Veins of the medulla oblongata, vv. meduuae oblongalae. Carry out the outflow of blood from the medulla oblongata and are tributaries of the anterior pontine cerebral vein. Rice. IN.
  17. Vein of the lateral pocket of the fourth ventricle, v. recessus lateralis ventriculi quarti. A tributary of the inferior petrosal sinus. Rice. IN.
  18. Veins of the cerebellum, vv. cerebelli.
  19. Upper vein of the worm, v. superior vermis. It starts from the upper part of the worm and flows into the large cerebral or internal cerebral veins. Rice. IN.
  20. Inferior vein of the worm, v. inferior vermis. It starts from the lower half of the cerebellar vermis and opens into a straight sinus. Rice. IN.
  21. Superior veins of the cerebellum, vv. superiores cerebelli. They depart from the lateral surface of the cerebellar hemisphere and open into the transverse sinus. Rice. A.
  22. Inferior sutures of the cerebellum, w. inferiores cerebelli. Collect blood from the lower and lateral surfaces of the cerebellar hemisphere. They are tributaries of the nearby sinuses of the solid meninges. Rice. IN.
  23. Precentral cerebellar vein, v. praecentralis cerebelli. It starts between the uvula and the central lobule. It empties into the great cerebral vein. Rice. B. 24a Stony Vein v. petrosa. In some cases, a large vessel that departs from the shred and flows into the upper or lower petrosal sinuses. Rice. IN.
  24. Eye veins, vv. orbitae.
  25. Superior ophthalmic vein, v. ophthalmica superior. Continuation of the nasolabial vein. It is located above and medially from the eyeball. It leaves the orbit through the superior orbital fissure and flows into the cavernous sinus. Rice. B.
  26. Nasal vein, v. nasofrontal. It is located between the superior shaw vein on one side and the junction of the supratrochlear and occipital veins on the other. Rice. B.
  27. Ethmoid veins, vv. eihmoidales. Rice. B.
  28. Lacrimal vein, v. lacrimalis. Rice. B.
  29. Vorticose veins, vv. vorticosae (w. choroideae oculi). Four to five branches from the choroid that pass through the sclera on the lateral side of the eyeball. Rice. B.