Cerebral arteriovenous malformations are the most common type of cerebrovascular malformation and are located superficially or deeply in the brain. The malformed vessels are composed of arteries and veins, and some contain aneurysms and venous aneurysms. Cerebral arteriovenous malformations have both blood supplying arteries and draining veins and are of various sizes and shapes. Intracranial (and intravertebral) vascular malformations are congenital abnormalities of central nervous system vascular development and can be divided into five types.
① arteriovenous malformation (AVM);
②Spongy hematoid osteoma;
(iii) Capillary dilation;
④Venous malformation;
⑤ varicose veins. Among the above five types of vascular malformations, AVM is the most common, accounting for 62.7% of intracranial supratentorial vascular malformations. It accounts for 42.7% of submural vascular malformations.
AVM is a pathological mass of abnormal development of cerebral vessels. Its size can grow with human development. The aberrant vascular mass is composed of one or several curved and dilated arteries supplying blood and draining veins, with a small diameter of less than 1 cm and a large diameter of up to 10 cm. The aberrant vascular mass contains brain tissue, and the surrounding brain tissue is atrophied due to solid ischemia, with glial hyperplasia and sometimes old hemorrhages. The arachnoid membrane on the surface of the malformed vessels is white and thick.
Intracranial AVMs can be located anywhere in the cerebral hemisphere and are wedge-shaped with the tip pointing toward the lateral ventricles.
Symptoms and signs
1.Hemorrhage The rupture of the malformed vessel can lead to intracerebral, intraventricular and subarachnoid hemorrhage, resulting in impaired consciousness. Symptoms such as headache and vomiting may occur. However, the clinical symptoms of small hemorrhage are not obvious. Most of the hemorrhage occurs in the brain, and 1/3 causes subarachnoid hemorrhage, accounting for 9% of subarachnoid hemorrhage, depending on the intracranial aneurysm. Bleeding has been reported to be the first symptom in 30% to 65% of AVMs. The age of predilection for hemorrhage is 20-40 years. It is generally believed that single supply artery, small size, deep site. As well as posterior cranial fossa AVMs are prone to acute rupture and bleeding. The risk of AVM rupture increases in women during pregnancy. Recent studies have found that the annual bleeding rate of unruptured AVMs in all age groups is about 2%. The risk of AVM bleeding is higher in younger patients than in older patients, and the rate of rebleeding and post-bleeding mortality are lower in AVMs than in intracranial aneurysms. This is due to the fact that the source of hemorrhage is mostly a vein of pathological circulation with lower pressure than cerebral arterial pressure. In addition, hemorrhage is less likely to occur in the basal pool, and cerebral vasospasm secondary to hemorrhage is rare.
2, convulsions in adults 21%-67% with convulsions as the first symptom, more than half occur before 30 years old, mostly in frontal and temporal AVM. frontal AVM mostly occurs convulsions of grand mal seizures, the top is mainly limited seizures. AVM occurs convulsions related to cerebral ischemia, progressive gliosis around the lesion, and stimulation of the cerebral cortex by iron-containing hemoglobin after bleeding. 14%-22% of AVM with bleeding will Convulsions occur. Early convulsions can be controlled with medication, but eventually medication is ineffective and convulsions are difficult to control. As a result of long-term intractable seizures, the lack of oxygen to the brain tissue is aggravated, resulting in the patient’s mental retardation.
3. Headache Half of the AVM patients have a history of headache. The headache can be unilateral and localized, or total headache. Intermittent or migratory. The headache may be related to the dilatation of the blood supply arteries, drainage veins and sinuses, and sometimes to the small amount of hemorrhage, hydrocephalus and increased intracranial pressure in AVM.
4, neurological deficits Among AVMs with unruptured hemorrhage, 4%-12% have acute or progressive neurological deficits. Intracerebral hemorrhage can cause acute neurological deficits. Due to the effect of AVM blood theft or combined with hydrocephalus. Patients have progressive neurological deficits, manifesting as motor, sensory, visual field and speech dysfunction. Individual patients may have cranial murmur or trigeminal neuralgia.
5, Children with large venous malformation of the brain, also known as large venous aneurysm of the brain, can lead to heart failure and hydrocephalus.
Diagnostic tests
1.CT of the head After enhanced scan AVM shows a mixed density area, and the midline structure of cerebral hemisphere is not displaced. In the acute bleeding period, CT can determine the site and extent of bleeding.
2.MRI of the head can show the high speed blood flow in the lesion as flow-void phenomenon, in addition, MRI can show the good relationship between the lesion and brain anatomy, which can provide the basis for choosing the surgical access for resection of AVM.
3.Cerebral angiography is the necessary means to confirm the diagnosis of this disease. Whole brain angiography and continuous filming. It is possible to understand the size and scope of the malformed vascular mass, the blood supplying artery, the draining vein and the blood flow rate, and sometimes it is also possible to see the phenomenon of blood steal from the contralateral internal carotid artery or vertebrobasilar artery system.
4.Electroencephalography Slow waves or spike waves may appear in and around the lesioned area of the affected cerebral hemisphere. Intraoperative EEG monitoring of patients with convulsions and removal of the epileptic lesion may reduce postoperative convulsive seizures.
Treatment options
1. Surgical resection is the most fundamental method for treating intracranial AVM, which not only eliminates rebleeding of the lesion, but also stops the phenomenon of blood theft from the malformed vessels, thus improving cerebral blood flow. As long as the lesion is located in the surgically resectable area, craniotomy should be performed. With the application of microsurgical techniques, surgical resection of intracranial AVMs is satisfactory. In emergency patients with AVM bleeding and hematoma formation, cerebral angiography should be completed preoperatively if available to clarify the malformed vessels. If the patient has brain herniation and is not eligible for cerebral angiography, emergency craniotomy can be performed. First remove the hematoma to lower the cranial pressure. Rescuing life, and then removing the malformed blood vessel after the second stage surgery. It is dangerous to remove the malformed blood vessel without angiography.
2.Surgical resection is not suitable for AVM located in deep brain important functional areas such as brainstem and mesencephalon. If the residual AVM is less than 3cm in diameter after surgical resection, Y-knife or X-knife treatment can be considered to make the endothelium of the malformed vessel slowly proliferate and the vessel wall thicken. The thrombus is formed and occluded, but during the treatment period. There is still a possibility of bleeding.
3.Embolytic therapy: Embolization of the blood supply artery reduces the risk of rupture and bleeding, and alleviates the symptoms caused by “blood theft”. The AVM is embolized with special synthetic rubber, balloon and other materials to reduce its size, and then surgically removed. Interventional treatment can sometimes cure some AVMs with a single arterial supply.
Cerebral angiography should be reviewed after all kinds of treatment to see if the malformed vessels have disappeared. The remaining malformed vascular mass should be treated with other treatments to avoid rebleeding.