Arteriovenous Malformation (TAAF)
An arteriovenous malformation (AVM) is a complex tangle of abnormal arteries and veins linked by one or more direct connections called fistulas or shuts.
This tangle of abnormal arteries and veins is referred to as a nidus. Normally, as the high-pressure arterial blood is pumped through a capillary bed there is a gradual decrease in blood pressure before reaching the venous system. With an AVM, the capillary bed is absent and the high-pressure arterial blood bypasses normal brain tissue and is pumped directly into the normally low-pressure venous system.
There is typically high blood flow through the nidus of the AVM, but it is not known whether the flow is a cause or effect of the abnormal blood vessels, or both. One thought is that the high-pressure blood from the arterial system gravitates towards the path of least resistance. Another thought is that the AVM itself recruits blood vessels.
Ultimately, the arterial blood rushes through the AVM, instead of working through available capillary beds, which feed the surrounding brain tissue, increasing blood flow through the nidus. This re-direction of the arterial blood away from the brain tissue and through the AVM is referred to as shunting.
Over time, the high blood flow and shunting of high-pressure arterial blood through the AVM causes the feeder arteries and veins making up the AVM to dilate (or expand). This dilation weakens veins making them susceptible to hemorrhage; feeder arteries become susceptible to aneurysms, a weakened spot in the blood vessel wall that expands and can eventually hemorrhage. A hemorrhage in the brain is a type of stroke in which a blood vessel ruptures and bleeds into the surrounding brain. For more information on strokes, please visit the American Stroke Association at www.strokeassociation.org.
There is a 10-15 percent risk of death, and a 20-30 percent chance of permanent brain damage, related to each bleed. Each time blood leaks into the brain, normal brain tissue is damaged. This results in loss of normal function, which may be temporary or permanent. Some possible symptoms include arm or leg weakness/paralysis, or difficulty with speech, vision, or memory. The amount of brain damage depends upon how much blood has leaked from the AVM (Higashida).
Smaller AVMs present with hemorrhage more often than large ones. In addition, the size of the hematoma (a localized swelling filled with blood resulting from a break in a blood vessel) is larger from the small AVM, compared with the medium or large AVM. There appears to be no difference in the frequency of hemorrhage between large and medium AVMs. However, whether size of the AVM is a true risk factor is unclear.
The structure of the abnormal vessels varies between what is usually found in arteries and that of veins. The tissue in and around the abnormal vessels is usually a kind of scar or fibrotic tissue (gliotic), but sometimes brain tissue is also found in some regions of the AVM.
AVMS arise in the brain, spine, lungs, kidneys, and skin. Brain AVMs are the most common and can occur anywhere in the brain. When an AVM occurs in the dura mater of the brain (the outermost lining of the brain), this is called a dural arteriovenous fistula (DAVF).
AVMs are thought to be congenital (that is, present at birth), arising from developmental derangements at the embryonic stage of vessel formation, at the fetal stage. However, this has never been clearly established and they may arise after birth. AVMs are usually single, except when associated with hereditary hemorrhagic telangiectasia (HHT). For more information on causes of AVMs, please visit the Causes of AVMs section.