A brain aneurysm involves the arteries at the base of the brain, specifically a ring of connected blood vessels called the Circle of Willis. Most aneurysms form where these arteries branch or connect, because those junction points endure the greatest physical stress from blood flow. Understanding which structures are involved helps explain why aneurysms form where they do, what happens when they grow, and why a rupture can be so dangerous.
The Circle of Willis
The Circle of Willis is a loop of arteries on the underside of the brain that distributes blood from the neck’s major vessels to every region of brain tissue. It connects the two internal carotid arteries (which supply the front of the brain) with the vertebral and basilar arteries (which supply the back). Small “communicating” arteries bridge the gaps between these larger vessels, creating a circular backup system so blood can reroute if one pathway becomes blocked.
Aneurysms cluster at very specific points along this ring. In imaging studies, roughly 59% of unruptured aneurysms sit along the internal carotid artery. About 15% appear where the internal carotid meets the posterior communicating artery, 9.5% at the middle cerebral artery, and 8.6% at the anterior communicating artery. A small percentage occur along the vertebral artery or the anterior cerebral artery. What all these locations share is a branching point or junction where blood flow changes direction, creating mechanical stress on the vessel wall.
How Blood Flow Weakens Artery Walls
Arteries are not simple tubes. They have three layers: an inner lining (the intima), a muscular middle layer (the media), and a tough outer wrapping (the adventitia). Between the intima and the media sits a thin sheet of elastic tissue called the internal elastic lamina. This elastic layer gives the artery its structural resilience, allowing it to stretch and snap back with each heartbeat.
At branching points along the Circle of Willis, blood decelerating or changing direction converts its velocity into pressure against the vessel wall. Over time, this hydraulic stress damages the internal elastic lamina. When segments of this elastic sheet break apart or disappear entirely, the wall loses its ability to resist outward pressure. The muscular middle layer can also degenerate at these spots. With both the elastic layer and the muscle layer compromised, the artery wall balloons outward, forming an aneurysm. Animal experiments have confirmed this directly: destroying the intima and elastic layer at a carotid bifurcation in rats produces an aneurysm almost immediately.
The relationship between blood flow and wall damage is a feedback loop. High shear stress from turbulent flow initially triggers cells lining the artery to produce enzymes that degrade the elastic layer. Once a small bulge forms, the flow pattern inside it changes. The dome of the aneurysm experiences persistently low shear stress, which causes the lining cells to die off, further weakening the wall. As the aneurysm grows, the area of low shear stress expands, accelerating the process.
Types and Shapes of Brain Aneurysms
About 90% of brain aneurysms are saccular, also called berry aneurysms. These look like a small round pouch attached to the artery by a narrow neck, the way a berry hangs from a stem. The pouch forms on one side of the vessel, typically at a fork. A saccular aneurysm is a “true” aneurysm, meaning all three wall layers are present, though they are stretched and thinned.
Fusiform aneurysms are much less common in the brain. Instead of bulging to one side, the entire circumference of the artery swells outward over a stretch of the vessel, creating a spindle shape. These tend to involve longer segments of artery wall degeneration rather than a single weak spot at a fork.
Two other types are defined by their cause rather than their shape. Dissecting aneurysms form when blood enters a tear in the inner wall and splits the layers apart. Mycotic aneurysms result from an infection that weakens the artery wall, often from bacteria traveling through the bloodstream. A pseudoaneurysm, or false aneurysm, is a contained leak where only the outer layer of the artery holds the blood in place.
Size Categories
Aneurysms under 10 mm in diameter are classified as small. Those between 10 and 25 mm are large, and anything over 25 mm is considered giant. Most aneurysms found incidentally on brain scans are small. Size matters because it influences both rupture risk and which nearby structures the aneurysm may press against as it grows.
Nearby Nerves and What They Control
The arteries of the Circle of Willis run close to several cranial nerves, and an expanding aneurysm can compress them. The most clinically significant example involves the third cranial nerve, which controls most eye movements, the upper eyelid, and pupil size. Aneurysms at the junction of the internal carotid and the posterior communicating artery sit right next to this nerve. When they grow or begin to leak, the pressure causes a distinctive set of symptoms: the eyelid droops, the eye drifts outward and downward (because the muscles that pull it inward and upward are paralyzed), and the pupil becomes fixed and dilated. This combination is a well-known warning sign that an aneurysm may be compressing the nerve.
Aneurysms that develop within the cavernous sinus, a venous channel alongside the sphenoid bone behind the eyes, can affect multiple nerves at once. The fourth cranial nerve (which fine-tunes downward eye movement), the sixth cranial nerve (which moves the eye outward), and the first branch of the fifth cranial nerve (which carries sensation from the forehead) all pass through this space. Damage here typically produces double vision and facial numbness together.
What Happens When an Aneurysm Ruptures
The brain is surrounded by three membranes called meninges. The innermost layer, the pia mater, clings directly to the brain’s surface. The middle layer, the arachnoid, is separated from the pia by a thin space filled with cerebrospinal fluid. The arteries of the Circle of Willis run through this subarachnoid space, so when an aneurysm ruptures, blood pours directly into it.
This is a subarachnoid hemorrhage. Blood spreads through the fluid-filled channels, called cisterns, that surround the brain. The specific cisterns affected depend on where the aneurysm sits. For example, a ruptured aneurysm on the anterior communicating artery sends blood into the cisterns between the frontal lobes, while bleeding from a posterior artery pools in the cisterns around the brainstem (the perimesencephalic cisterns). Blood can also flow into the brain’s internal fluid chambers, the ventricles, particularly reaching the fourth ventricle near the brainstem. When this happens, the blood irritates the meninges and causes intense neck stiffness and headache.
The pooled blood creates problems beyond the initial bleed. It can block normal cerebrospinal fluid drainage, causing pressure to build inside the skull. It can also trigger spasms in nearby arteries days later, reducing blood supply to brain tissue that was unharmed by the original hemorrhage.
Genetic and Connective Tissue Factors
The structural integrity of artery walls depends heavily on the proteins that make up connective tissue. Several inherited conditions that weaken these proteins carry a significantly higher risk of brain aneurysms. In the general population, about 3.2% of people have an intracranial aneurysm. Among people with connective tissue disorders, that prevalence jumps to between 9% and 28%.
Marfan syndrome affects a protein called fibrillin that gives connective tissue its elasticity. Ehlers-Danlos syndrome involves defects in collagen, the main structural protein in vessel walls. Loeys-Dietz syndrome disrupts signaling molecules that regulate how blood vessel walls grow and repair themselves. Neurofibromatosis type 1 affects a protein involved in cell growth regulation. In all four conditions, the arterial walls are inherently weaker, making the elastic layer and muscular layer more vulnerable to the normal hemodynamic stresses that healthy arteries can withstand for a lifetime.
Even without a named genetic syndrome, having a first-degree relative with a brain aneurysm increases your own risk, suggesting that subtler inherited differences in vessel wall composition play a role in many cases.