Brain arteriovenous malformation

Introduction to brain arteriovenous malformation Arteriovenous malformation (AVM) is the most common type of malformation caused by abnormal cerebral vascular development. Accounted for more than 90% of cerebral vascular malformations. Malformed blood vessels are composed of arteries and veins, some include aneurysms and venous tumors, and there are blood supply arteries and drainage veins in cerebral arteriovenous malformations, which vary in size and shape. The disease can occur in any part of the brain, and the left and right sides of the lesion are roughly equal. More than 90% are located on the cerebellum, and most are distributed in the cerebral cortex, accounting for about 70% of the on-screen lesions. Among them, the top, the forehead and the temporal lobe are more common, and the occipital lobe is slightly less. Cerebral arteriovenous malformation is a congenital disorder, which is formed by the cerebral angiogenesis during embryonic development. It is generally believed that it occurs at the 45th to 60th day of the embryo. At the 4th week of the embryo, the primordial vascular network begins to form. The original blood circulation occurs, and the original blood vessels re-differentiate the arteries, veins and capillaries. In the early embryonic stage, the original arteries and veins communicate with each other. Later, due to local capillary dysplasia, the arteries and veins still communicate directly. The form is left behind. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people. Mode of infection: non-infectious Complications: cerebral ischemic disease, brain atrophy, brain subarachnoid hemorrhage

Cause of cerebral arteriovenous malformation

(1) Causes of the disease

Cerebral arteriovenous malformation is a congenital disorder, which is formed by the cerebral angiogenesis during embryonic development. It is generally believed that it occurs at the 45th to 60th day of the embryo. At the 4th week of the embryo, the primordial vascular network begins to form. The original blood circulation occurs, and the original blood vessels re-differentiate the arteries, veins and capillaries. In the early embryonic stage, the original arteries and veins communicate with each other. Later, due to local capillary dysplasia, the arteries and veins still communicate directly. The form remains, because there is no resistance to normal capillaries, the blood flows directly from the artery into the vein, causing the vein to expand due to increased pressure. The artery is gradually thickened due to more blood supply, and the formation and expansion of the collateral vessels form a distortion. The vascular group with different thickness and thickness, the weakened part of the blood vessel wall expands into a saclike shape, and there is no capillary between the internal cerebral artery and the vein, which directly communicates to form a number of sacral tracts, and the blood flows from the blood supply artery into the deformed vascular group. Through the fistula straight into the vein, and then concentrated to 1 to several drainage veins, leaving the vascular mass, flow to the sinus, due to lack The capillary structure is deficient, resulting in a series of changes in cerebral hemodynamics with corresponding clinical signs and symptoms.

(two) pathogenesis

AVM often begins with symptoms caused by intracranial hemorrhage and brain stealing. The root cause of the disease is the lack of capillary structure between the arteries and veins in the AVM lesion. The arterial blood directly flows into the vein, and the blood flow resistance suddenly decreases, resulting in a decrease in regional cerebral arterial pressure. The cerebral venous pressure is increased, resulting in a series of hemodynamic disorders and pathophysiological processes.

Bleeding

A variety of factors can cause intracranial hemorrhage:

(1) The blood of a large flow distorts the arterial expansion of the abnormal wall structure, and the blood vessel wall is further damaged and destroyed, and the local rupture is bleeding once the blood flow pressure cannot be withstood.

(2) AVM-related aneurysm rupture and bleeding, with aneurysm lesion bleeding rate of 90% to 100%.

(3) A large amount of blood flow impinges on the drainage vein of the malformed vascular mass, and the thinner vein of the wall is locally expanded into a saclike or tumor-like shape, which is prone to rupture and bleeding.

(4) Because a large amount of blood passes through the arteriovenous fistula in the AVM, the artery is rapidly injected into the vein, and the local cerebral arterial pressure drops, resulting in the normal perfusion of the brain tissue around the lesion. The arterial blood flows to the AVM area, and the brain steals blood. "Phenomenon, long-term ischemia, the small arteries in the surrounding area are in an expanded state, and the wall structure changes accordingly. In some cases, such as when the whole body blood pressure rises rapidly, the dilated blood vessels may also have rupture and bleeding.

The size of AVM has a certain correlation with the risk of bleeding. It is generally believed that the small AVM (maximum diameter <2.5cm) has a relatively high bleeding rate, which may be due to the smaller diameter of the deformed blood vessels and the small decrease in arterial pressure. The wall is also thin, so under the impact of blood flow under higher pressure, the chance of blood vessel rupture is larger. On the contrary, the large (large diameter <5cm) blood vessel has larger diameter, the arterial pressure drops larger, and the blood vessel wall is thicker. It can withstand high blood flow pressure and the chance of rupture is small.

The location of AVM also has a certain relationship with bleeding tendency. The lesions in deep lesions such as ventricles, ventricles, basal ganglia, thalamus, and insula are higher than hemisphere AVM, up to 1.5 times, especially in the ventricles or ventricles. The bleeding rate of the lesion is higher. The reason may be that the deep lesion is generally small, the blood supply artery is short, the caliber is small, the arterial pressure is high, and the AVM is easy to rupture. At the same time, the drainage vein of the deep AVM is often a deep vein, and the deep vein has a chance of stenosis. It is easy to cause venous hypertension, causing rupture of vein or AVM group, especially the lesion with deep venous drainage. The AVM located in the ventricle or ventricle is also prone to hemorrhage due to lack of support of brain tissue around it. It is often intraventricular hemorrhage. .

2. Brain stealing blood

The range of cerebral ischemia caused by stealing blood is larger than the range of deformed vascular mass. The resulting symptoms and signs are also more extensive than the corresponding functional changes in the lesion area. The severity of stealing blood is related to the size of AVM. The greater the amount of stealing blood, the more severe the cerebral ischemia, the small amount of AVM stealing blood, the milder cerebral ischemia, or even the ischemia, there is no clinical symptoms, severe ischemia can cause epilepsy or transient Cerebral ischemic attack or progressive neurological deficit, such as somatosensory or hemiplegia.

3. Brain hyperperfusion

A large amount of brain stealing blood expands blood vessels in adjacent brain tissue to obtain more blood flow to supply brain tissue, so that the long-term expansion of the arterial wall gradually weakens, the wall becomes thinner, and the auto-regulation function of blood vessels decreases, the threshold The upper limit is reduced, even in a paralyzed state. Once the cerebral perfusion pressure rises above the upper limit of the cerebral vascular autoregulation threshold, the arteries with autoregulatory dysfunction not only do not contract but instead expand acutely, and cerebral blood flow increases linearly with perfusion pressure. , that is, the occurrence of brain hyperperfusion, manifested as elevated local venous pressure, peripheral cerebral venous blood flow blocked and sudden brain swelling, cerebral edema, increased intracranial pressure, extensive small blood vessel rupture and other phenomena, especially in The huge-type high-flow AVM (maximum diameter >6cm) is very easy to occur after resection. It is reported in the literature that the incidence of brain hyperperfusion is 1% to 3% after the large and medium-sized AVM, and the huge AVM is 12% to 21%. Its disability and mortality rate is as high as 54%. This phenomenon can also occur in AVM's endovascular intervention and is the most serious risk that may occur during AVM treatment.

AI-Rodhan (1993) presented another explanation for cerebral edema and residual venous bleeding after AVM. It is believed that the stump stenosis, thrombosis or embolism of the drainage vein after AVM resection, and venous return obstruction of surrounding brain tissue Venous occlusive congestion

4. Increased intracranial pressure

AVM itself has no placeholder effect, but many patients show signs of increased intracranial pressure. On the one hand, arterial blood directly enters the vein in AVM, which leads to increased cerebral venous pressure, hinders venous return of surrounding brain tissue and causes long-term congestion of brain tissue. Edema, increased intracranial pressure; on the other hand, AVM patients are often accompanied by hydrocephalus, the cause of hydrocephalus may be the drainage of deep veins deep in the brain, enlargement into a spherical venous tumor or intraventricular hemorrhage blocked cerebrospinal fluid circulation. It can also be caused by cerebral venous hypertension affecting the absorption or bleeding of cerebrospinal fluid, causing partial occlusion of the subarachnoid space or blockage of arachnoid granules to reduce the absorption of cerebrospinal fluid, which can cause obstructive or traffic hydrocephalus; Intracerebral hematoma and cerebral edema around the hematoma are also important causes of increased intracranial pressure.

5. Pathology

Brain AVM can occur in any part of the brain, 80% to 90% is located on the screen, the top of the cerebral hemisphere surface, especially the middle cerebral artery supply area, the outer side of the temporal lobe is the most common, followed by the anterior cerebral artery supply area. The frontal lobe and the inner side of the brain, other parts of the occipital lobe, basal ganglia, thalamus, cerebellum, brainstem, corpus callosum, less common in the ventricle, the supratentorial lesions are mostly supplied by the middle cerebral artery or the anterior cerebral artery, and the AVM under the cerebellum is mostly from the cerebellum. Arterial blood supply or cerebellar anterior or posterior inferior arteries supply blood, there is only one blood supply artery, more than two or three, reflux veins are more than one, occasionally two, blood supply artery and reflux veins are coarser than normal, veins According to the statistics, the middle cerebral artery of the blood supply artery accounts for 60%, the branch of the anterior cerebral artery accounts for 20%, and the combined blood supply of the middle cerebral artery and the anterior cerebral artery accounts for 10%. The choroidal artery and the vertebral-basal artery branch provide blood. Rarely, the branch of the posterior cerebellum is about 2%. The reflux vein is connected to the sagittal sinus, the great cerebral vein, the parasagittal plexus, the sinus, the transverse sinus, the straight sinus, the supraspinal sinus, etc. due to the embryo. The cerebral blood vessels first develop in the soft brain membrane. Therefore, the arteriovenous malformation is often located on the surface of the brain. It can also be located in the sulci or in the deep brain tissue. The typical cerebral arteriovenous malformation is conical, the cone bottom is on the brain surface, and the cone tip is toward the ventricle. Deep into the ventricle wall, some extend into the ventricle and connect to the choroid plexus of the lateral ventricle. A few arteriovenous malformations are spherical, long or irregular, and the edges are not neat.

The size of the deformed vascular mass varies, and the disparity is very large. The small one can only be seen under careful examination. The cerebral angiography can not be displayed. It can only be found in the postoperative pathological examination, and some even the routine pathological examination is difficult to find. Large lesions can reach more than 8~10cm in diameter, which can affect more than two lobes, accounting for 1/3~1/2 of the cerebral hemisphere or widely distributed in one or both sides of the brain or cerebellar hemisphere. The deformed blood vessels in the lesion are entangled. In a cluster, the diameter of the vessel is different, sometimes small, sometimes extremely dilated, distorted, and even its stroke is distorted, spiral or rounded, and different sizes of arteriovenous capillaries are intertwined, and brain tissue can be interposed. .

Under the microscope, the characteristics of arteriovenous malformation are composed of different sizes and different arteries and veins. The lumen is dilated, the intima hyperplasia of the wall arteries is hypertrophic, and some of them protrude into the lumen. The inner elastic layer is extremely weak or even missing. The middle layer is different in thickness, and the atherosclerotic plaque and mechanical blood clot can be attached to the arterial wall. Some of the lumens are blocked, some are aneurysmal-like dilatation, and the veins often have fibrosis or glass-like changes. Thick, occasionally calcified, but the arteries and veins are often difficult to distinguish, there are common hemosiderin deposition around the deformed blood vessels, and the cerebral tissue variability necrosis between the blood vessels.

Because there are no capillaries between arteries and veins of arteriovenous malformation, blood flows directly into the vein through the artery, lacks vascular resistance, local blood flow increases, and blood circulation speed increases. This blood flow changes, causing a large number of "brain stealing" phenomenon due to arteries. The blood directly flows into the vein, causing the intra-arterial pressure to drop drastically. The intra-arterial pressure of the blood supply is reduced from the normal arterial circulation by 90% to 45.1% to 61.8%, and the venous pressure rises, causing the venous return in the lesion to be blocked. Induced venous engorgement, distortion, decreased arterial pressure, and "cerebral ischemia" phenomenon, the arterial autoregulation function is lost, causing the arteries to dilate, to compensate for the lack of blood supply to the distal brain, and the impact of blood flow in the arteries causes aneurysms to form. As well as long-term angulation, distortion, and formation of huge venous tumors, which are the factors of rupture of arteriovenous malformation, rapid blood flow in the vein, thickening of the blood vessel wall, arterial blood in the vein, and the vein is bright red during surgery. The arteries are difficult to distinguish. This is called the arterialization of the vein. With the expansion of the arteries and veins, the amount of blood stealing increases, and the range of lesions gradually expands. Big.

Cerebral arteriovenous malformation prevention

1, should choose a light, high-protein, high-calorie, easy to digest, rich in crude fiber low-fat diet.

2, eat more crude fiber food, keep the stool smooth.

3, quit smoking and alcohol, fasting spicy, cold and other irritating foods and excitatory drinks.

4, fasting 8 to 10 hours before surgery, banned drinking for 6 to 8 hours.

5, 6 hours after anesthesia awake, no swallowing disorder can enter a small amount of liquid diet, and gradually changed to soft food.

6, patients with high blood pressure, adhere to the medication under the guidance of a doctor. Do not arbitrarily change the dose or stop taking the drug to avoid blood pressure and induce bleeding.

Compassion complications Complications Cerebral ischemic disease Brain atrophy Brain subarachnoid hemorrhage

Secondary changes in cerebral arteriovenous malformations, the most common are abnormal blood vessel destruction, hematoma formation, thrombosis of abnormal blood vessels, cerebral ischemia, gliosis, brain atrophy, etc., abnormal vascular rupture often manifests as subarachnoid hemorrhage, Intracerebral hemorrhage, subdural hemorrhage, intraventricular hemorrhage, intracerebral hemorrhage often caused by deep arteriovenous malformation, and hematoma formation, manifested as a change in the position of vascular translocation, also visible photoinjection spillovers and arterial spasm, brain Ischemia can be caused by "brain stealing blood", which causes the brain tissue in the ischemic area to shrink and the gliosis to proliferate.

Symptoms of cerebral arteriovenous malformation Common symptoms Sensory disorder coma hydrocephalus intracranial pressure increased convulsions

1. Clinical classification and classification

There is no uniform standard for AVM classification. The following three classification methods are introduced:

(1) Classification according to AVM group size: At present, Drake (1979) standard is usually divided into: 1 small, maximum diameter <2.5cm; 2 medium, maximum diameter is 2.5~5.0cm; 3 large, maximum diameter >5cm, such as maximum The diameter is >6cm, which can be classified into a huge type.

(2) According to the morphological classification of angiography: Parkinson et al (1980) divided AVM into: 1 multi-unit type, with multiple arterial blood supply and multiple venous drainage, and there are many arteriovenous fistulas in the vascular group, the most common. 82%; 2 unit type, a small AVM with a blood supply artery and a drainage vein to form a fistula, accounting for about 10%; 3 straight type, one or several blood supply arteries directly into the large vein or vein of the brain Sinus, accounting for about 3%; 4 complex type, intracranial and extracranial arteries are involved in blood supply, reflux can also be through the intracranial and extracranial sinus, rare.

(3) Classification according to the three-dimensional shape of AVM: Shi Yuquan (1982) classified the AVM of 65 cases of plastic casting into a body model according to the shape, which was divided into: 1 varicose type, thickened and dilated cerebral artery and cerebral veins were wound into a group. There are many arteriovenous fistulas in the group. This type is the most common, accounting for 65%. 2 type, arteries such as dendritic, its branches directly coincide with the vein; 3 arteriovenous type, arteriovenous enlargement is balloon-like, whole The group AVM is like a ginger tuber; 4 mixed type, the above three types coexist in one lesion, and the latter three types each account for about 10%.

The clinical grading of AVM is necessary for formulating treatment plans, determining the surgical objects and methods, predicting the degree of difficulty during surgery, estimating the postoperative results, and comparing the advantages and disadvantages of various treatment methods and surgical methods. Shi Yuquan (1984) developed An AVM four-standard grading method, according to cerebral angiography, the AVM size, location, blood supply artery and drainage vein are divided into four grades (Table 1), if there are two factors are A certain level is defined as this level; if only one factor score is higher than the other three, then the item is reduced by half, and the application of the neurosurgery of Shanghai Huashan Hospital for many years proves that the Shis classification method is simple and practical. In 1986, the classification method developed by Spetzler and Martin rated the size (maximum diameter), location and drainage vein of AVM as the main indicators as O~3 points, and then comprehensively divided into 6 levels, of which the part was in the neurological function area. Such as feeling, motor cortex, language center, visual center, thalamus, internal capsule, deep cerebellum, cerebellar foot and other adjacent areas, 1 point; such as the brain stem and hypothalamus Enter level 6; other parts are 0 (Table 2), the sum of the three indicators scores, that is, the level of AVM (Table 3), there is only one combination of level I and level V, respectively, level II and level IV respectively There are 4 combinations in the class III, and the level VI is related to the brainstem and hypothalamus. This kind of grading method is widely used in the world, and is similar to the Shis grading method. The SpetzleI grading method is grade I and Shis grading. The level 1 is equivalent to the level 1.5, the former level II and the latter level 2, level III and level 2.5, IV, V level and level 3, 3.5 are equivalent, I, II level AVM surgery is less difficult to remove, no death The rate is even non-disruptive, and the higher the level, the higher the disability rate and the mortality rate.

2. Clinical signs and symptoms

Small arteriovenous malformations can be free of any symptoms or signs. Most arteriovenous malformations can have certain clinical manifestations. Common symptoms and signs are:

(1) Bleeding: The incidence rate is 20% to 88%, and most of them are the first symptoms. The smaller the arteriovenous malformation, the more likely it is to bleed. It usually occurs in young people, and the onset is sudden, often in the case of physical activity or emotional agitation. Severe headache, accompanied by vomiting; consciousness can be awake, there may be varying degrees of disturbance of consciousness, and even coma; there may be symptoms of meningeal irritation such as neck stiffness, and may also have neurological impairment such as increased intracranial pressure or hemiplegia and partial sensory disturbance. Performance, if the vascular rupture of the superficial brain of AVM can cause subarachnoid hemorrhage (SAH); if the rupture is deeper blood vessels, it will cause intracerebral hematoma; AVM rupture in the adjacent ventricle or ventricle is often in the brain. Hematoma is associated with intraventricular hemorrhage or intraventricular hemorrhage. AVM hemorrhage is more common in vascular rupture of blood vessels in the brain parenchyma, which causes many opportunities for intracerebral hematoma. Therefore, there is usually no risk of intracranial aneurysm bleeding, and the latter is mostly located in the cerebral artery ring. When the blood is ruptured, the blood is filled in the subarachnoid space of the skull base, causing severe cerebral artery spasm. 80% to 90% of the patients with AVM first bleeding can survive, and the survival rate of the first hemorrhage of the aneurysm is only 5 0% to 60%, AVM bleeding can also be repeated, up to more than 10 times, and as the number of bleeding increases, symptoms and signs increase, the condition deteriorates, comprehensive literature, unruptured AVM will have 2% to 4 per year % bleeding rate, and the risk of re-bleeding in the first year of ruptured bleeding AVM is about 6%, and 2% to 4% re-bleeding every year from the second year, the same as unruptured, secondary to bleeding The mortality rate is 1%, the total mortality rate is 10% to 15%, and the permanent severe disability rate is 2% to 3% per year, of which 20% to 30% is caused by hemorrhage. It can be seen that the unbleeded AVM and the over-blooded blood. The AVM has potential or real dangers to the health and life of the patient and must be given high priority.

(2) convulsions: About half of the patients have seizures, which are characterized by large seizures or focal seizures. AVM convulsions with frontal, parietal and temporal lobes are the most common, especially large, large-volume AVM patients with epilepsy. The onset may be the first symptom, or it may occur in hemorrhage or hydrocephalus. The incidence is related to the location and size of arteriovenous malformation. The incidence of epilepsy in the frontal region is the highest, reaching 86%. 85%, parietal lobe is 58%, temporal lobe is 56%, occipital lobe is 55%. The greater the arteriovenous malformation, the higher the incidence, the higher the incidence of large-scale arteriovenous malformation epilepsy with severe "brain stealing blood".

(3) Headache: More than half of the patients have a history of long-term headaches, similar to migraine, limited to one side, can be relieved by themselves, generally manifested as paroxysmal atypical migraine, may be related to cerebral vasodilation, headache is more common when bleeding Severe, with vomiting.

(4) progressive neurological dysfunction: the incidence of about 40%, mainly for exercise or sensory dysfunction, often occurs in larger AVM, due to a large number of brain stealing blood caused by cerebral ischemic attack, hemiparesis or limb numbness, The initial transient episode, with the increase in the number of episodes, can be aggravated and become permanent. In addition, multiple hemorrhages in the brain can also cause aggravation of neurological damage. The brain tissue of long-term ischemia caused by brain stealing increases with age. The cerebral arteries are extensively hardened or thrombotic. The progression of brain atrophy is faster than that of normal people, and the progressive development of neurological dysfunction is faster and heavier.

(5). Other giant types, especially AVM involving bilateral frontal lobe may be associated with mental retardation. Epilepsy and anti-epileptic drugs may also affect mental development or promote the development of mental retardation. Larger AVM involves extracranial or dura mater When the patient consciously had a murmur in the skull, the AVM under the curtain, except for SAH, had fewer symptoms and was not easy to find.

Examination of cerebral arteriovenous malformation

There was no significant change in cerebrospinal fluid before lumbar puncture bleeding. The intracranial pressure after hemorrhage was between 1.92 and 3.84 kPa, and the cerebrospinal fluid was homogeneously bloody, suggesting subarachnoid hemorrhage.

Intracranial plain film

Most patients have no positive findings, 10% to 20% of cases with lesion calcification, 20% to 30% of calcification is linear, ring-shaped, plaque or irregular, the image is often very light, if the middle meningeal artery participates in blood supply, visible skull The middle cerebral artery sulcus is widened, the skull base is enlarged like a spinous hole, and the obstructive hydrocephalus caused by arteriovenous malformation in the posterior cranial fossa can show signs of increased intracranial pressure. After the hemorrhage, the pineal calcification shift can be seen.

2. EEG

Most patients may have abnormalities in EEG, mostly localized abnormal activities, including the reduction or disappearance of rhythm, slowing of wave rate, lower amplitude, sometimes diffuse wave, and intracerebral hematoma. The focal delta wave, the underlying arteriovenous malformation often has irregular slow waves. About 50% of patients with epilepsy history may have epileptic waveforms, and EEG abnormalities occur in the same side of the lesions, accounting for 70% to 80%. A small number of patients with cerebral hemisphere arteriovenous malformations may present bilateral EEG abnormalities. This is due to the phenomenon of "brain stealing blood", which causes epilepsy caused by contralateral cerebral hemisphere ischemia and deep small vascular malformation. Stereoscopic EEG can trace accurate epileptic foci.

3. Isotope scanning

About 90% to 95% of the supratentorial arteriovenous malformation is a positive result. Generally, 99Tc or 197Hg is used for scintigraphy and continuous imaging. More localization diagnosis can be made, which is characterized by isotope accumulation, but arteriovenous diameter less than 2cm. Malformations are often difficult to find.

4. Head CT scan

AVM with unbleeded CT scan showed irregular low, equal or high-density mixed lesions, which may be in the form of a mass, which may also be patchy, with unclear boundaries. The internal high density may be fresh small bleeding points, including Hemosiderin, gliosis, thrombosis or calcification, generally no mass effect, no obvious signs of cerebral edema around, after injection of contrast agent, it shows obvious spot-like or lumpy enhancement, sometimes visible connected with vascular mass Distorted blood supply artery or drainage venous angiography, brain atrophy, ventricular enlargement or hydrocephalus around the lesion, CT scan of intracranial hemorrhage can be seen in subarachnoid hemorrhage or intracerebral hematoma, may also be associated with intraventricular hemorrhage Hematoma in the brain parenchyma often has a sign of occupation (Fig. 1). The surrounding brain tissue is edematous, the ventricle is compressed, displaced, and even the midline is moved to the opposite side.

5. Skull MRI imaging

MRI is of particular value in the diagnosis of AVM. In general, fast-flowing blood, in the form of eddy currents, on the MRI image, either T1-weighted or T2-weighted, has a low-signal or no-signal tubular or polka-like shape. The vascular shadow, AVM appears as a mass or plaque-like lesion consisting of such "empty" vascular shadows (Fig. 2), with irregular borders, often showing large blood supply arteries and drainage veins in and out of the vascular mass, injection After the enhancer, some vascular shadow enhancement, MRI diagnosis of the posterior fossa AVM is significantly better than CT, it does not have the effect of skull artifacts, in addition, MRI images, can clearly show the AVM lesions and the surrounding important structures of the brain Adjacent relationships to compensate for the lack of cerebral angiography, providing more detailed information for the design of the surgical approach and estimation of prognosis.

6. Cerebral angiography

Cerebral angiography is the most important diagnostic tool for AVM. The digital subtraction angiography (DSA), which has been widely used, can obtain contrast images of clear continuous films. The characteristic performance of AVM is visible on the arterial phase. Or a number of abnormally thickened blood supply arteries go to a mass of irregular deformed vascular lesions, with dilatation, distorted drainage veins appearing early, cerebral cortex AVM drainage veins into the upper and lower sagittal sinus, transverse sinus, Most of the sigmoid sinus, deep lesions can be introduced into the straight sinus from the deep sinus, and then to the transverse sinus. The blood supply artery of the AVM can be from the anterior cerebral artery of the ipsilateral internal carotid artery, the branch of the middle cerebral artery, or the vertebral artery. The branch of the posterior cerebral artery; through the cerebral artery ring, the contralateral internal carotid artery or vertebral artery branch can also participate in blood supply, the under-the-shoulder AVM is mainly supplied by the branch of the vertebral artery system (Fig. 3), in addition, on the screen, under the curtain The lesions can accept the blood supply of the extracranial arterial system. Therefore, for AVM patients, routine whole brain angiography and even six angiography are necessary. The distal cerebral artery is often filled with blood. Or not filling, if there is a large intracerebral hematoma, there may be avascular zone, normal cerebral vascular dysfunction, the smaller AVM vascular mass is not developed by hematoma compression, after the hematoma is absorbed and then cerebral angiography Appearance, therefore, in patients with acute cerebral angiography without abnormal vascular group, should be followed up after 1 to 2 months to avoid missed diagnosis.

7. Three-dimensional computed tomography

Angiography (3D-CTA) and Magnetic Resonance Angiography (MRA) 3D-CTA and MRA are the result of the development of modern medical imaging equipment and advanced computer 3D reconstruction technology in recent years. 3D-CTA is the application of electron beam imaging system or spiral CT. The intracranial AVM after intravenous injection of contrast agent was scanned continuously, and the original image was collected and transferred to the graphic workstation. The maximum density projection method and surface occlusion method were used for 3D reconstruction. The obtained image was rotated at multiple angles to form a three-dimensional image. Structure, and cut the required image from different angles, MRA is the application of high field strength magnetic resonance instrument, using 2D-PC and 3D-TOF method for angiography, the original image is processed in the 3D reconstruction image of the graphic workstation, and 360° rotation.

The Department of Neurosurgery and Radiology of Shanghai Huashan Hospital has used 3D-CTA and MRA to observe brain AVM, and compared with DSA, 24 patients with AVM who underwent DSA, 3D-CTA and MRA, 3D-CTA positive diagnosis The rate can reach 100%, while MRA has about 4% false negative. The intracranial AVM images obtained by 3D-CTA and MRA can clearly show AVM vascular mass, mainly blood supply artery and drainage vein, both of which are non-invasive. The examination is simple, the cost is lower than the DSA, and the complications are few. The 3D-CTA describes the stereoscopic structure well and can show the relationship with the skull base structure; the scanning time is short, and it can be used for the acute bleeding examination, while the MRA does not need to be injected. Contrast agent, no radiation, vascular imaging resolution and clarity, but stereoscopic description is poor, although DSA is a traumatic examination, patients need to receive large doses of radiation and contrast agents, complications, but for all levels The display clarity of blood vessels and lesions is extremely high, and it is still the most important method for AVM diagnosis. However, the continuous improvement and development of 3D-CTA and MRA has broad application prospects.

8. Transcranial Doppler ultrasound

It can be detected from three parts: the middle cerebral artery, the end of the internal carotid artery, the middle cerebral artery, the end of the internal carotid artery, the anterior cerebral artery and the posterior cerebral artery through the ankle; the vertebral artery, the basilar artery and the cerebellum are detected through the large foramen magnum The lower arteries; the eye artery and the internal carotid artery siphon are detected by the eye. The blood flow velocity of the normal human brain is the fastest in the middle cerebral artery, which is followed by descending: the anterior cerebral artery, the internal carotid artery, the basilar artery, and the posterior cerebral artery. The vertebral artery, the ophthalmic artery, and the slowest blood flow velocity are the inferior cerebellar artery. With the increase of age, the average blood flow rate decreases. There is a significant difference between 21-30 years old and 61-70 years old (P<0.01). There is a vascular disease in one side of the hemisphere, which makes the blood flow velocity of the two hemispheres significantly different. The nature of the lesions is different, the blood flow velocity can be accelerated, and the blood flow velocity can be slowed down. When the blood vessels are in a paralyzed state, the blood flow velocity is obviously accelerated. When the blood vessels are occluded, the blood is blocked. The flow velocity is slowed down, and when there is an arteriovenous malformation, the blood flow velocity of the blood supply artery is accelerated.

Doppler ultrasound can be used to determine the direction of blood flow and arteriovenous malformation; to distinguish the inflow and outflow of arteriovenous malformation; the location of deep arteriovenous malformation; to dynamically monitor the blocking effect of arteriovenous malformation Hemodynamic changes, transcranial Doppler ultrasound combined with CT or MRI, contribute to the diagnosis of cerebral arteriovenous malformation, preoperative and intraoperative use of transcranial Doppler ultrasound for cerebral arteriovenous malformation Academic evaluation can avoid dangerous complications such as normal perfusion pressure breakthrough syndrome caused by hemodynamic changes during surgery.

Diagnosis and differential diagnosis of cerebral arteriovenous

diagnosis

Diagnosis of sudden subarachnoid hemorrhage under the age of 40, history of epilepsy or hemiparesis before hemorrhage, aphasia, headache history, and no significant increase in intracranial pressure, should be highly suspected of arteriovenous malformations, but the diagnosis depends on the brain Angiography, CT and MRI are helpful in confirming the diagnosis.

Differential diagnosis

Cerebral arteriovenous malformation needs to be differentiated from other cerebrovascular malformations, moyamoya disease, primary epilepsy, and intracranial aneurysms.

Cerebral cavernous hemangioma

It is also one of the common causes of repeated subarachnoid hemorrhage in young people. Patients with hemorrhagic disease often have no obvious clinical symptoms. Cerebral angiography is often negative or pathological vascular mass, but no thickened blood supply artery or dilated drainage can be seen. Intravenous, CT plain scan can be expressed as a low-density area of honeycomb, and the lesions are slightly enhanced after enhancement, but finally need surgical resection and pathological examination to distinguish from arteriovenous malformation.

2. Primary epilepsy

Cerebral arteriovenous malformations often occur epilepsy, and arteriovenous malformations of thrombosis are more prone to intractable seizures. At this time, cerebral angiography is often not developed, so it is often misdiagnosed as epilepsy, but primary epilepsy is common in children, for young people. Epilepsy, subarachnoid hemorrhage or epilepsy after subarachnoid hemorrhage should be considered as arteriovenous malformation. In addition, in addition to epilepsy, patients with arteriovenous malformations have other signs and symptoms, such as headache, progressive light Hemiplegia, ataxia, visual impairment, etc., CT scan helps differential diagnosis.

3. Cerebral aneurysms

It is the most common cause of subarachnoid hemorrhage. The age of onset is about 20 years older than that of cerebral arteriovenous malformation, that is, it is more common in 40 to 50 years old, and it is more common in women. Patients often have high blood pressure, history of arteriosclerosis, and seizures are rare. The oculomotor nerve palsy is more common, and it is not difficult to identify according to cerebral angiography.

4. Venous vascular malformations

Less common, sometimes ruptured bleeding caused by subarachnoid hemorrhage, and increased intracranial pressure, cerebral angiography without obvious deformed blood vessels, sometimes only a large vein with some drainage branches, CT scan shows low In the density zone, enhanced scans showed enhanced lesions.

5. Moyamoya disease

This disease is more common in children and young adults, children with cerebral ischemia as the main manifestation, adult with intracranial hemorrhage as the main symptom, clear differential diagnosis depends on cerebral angiography, moyamoya cerebral angiography showed internal carotid artery stenosis or occlusion, brain There is a cloud-like slender abnormal vascular mass at the base of the base.

6. Blood-rich brain tumors

Cerebral arteriovenous malformation still needs to be differentiated from blood-rich gliomas, metastases, meningioma and hemangioblastoma. Because of the abundant blood supply of these tumors, the communication between arteries and veins and early veins can be seen in cerebral angiography. Therefore, it will be confused with cerebral arteriovenous malformation, but according to the age of onset, medical history, course of disease, clinical symptoms and signs, etc., CT scan can help to distinguish the differential diagnosis.

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