About 85% of non-traumatic subarachnoid hemorrhages are caused by a ruptured brain aneurysm, a weak, balloon-like bulge in an artery on the brain’s surface. When this bulge bursts, blood spills into the space between the brain and the thin tissues surrounding it, creating sudden, intense pressure. The remaining cases stem from vascular malformations, drug use, blood vessel disorders, or causes that are never identified. Globally, subarachnoid hemorrhage affects roughly 8.3 people per 100,000 each year.
Ruptured Brain Aneurysms
A brain aneurysm is a spot where an artery wall has thinned and ballooned outward. Many people live with small aneurysms that never cause problems. But when one ruptures, blood floods the subarachnoid space at arterial pressure, and the result is a medical emergency. The hallmark symptom is what doctors call a thunderclap headache: an extraordinarily severe headache that reaches peak intensity in under a minute. Among people who arrive at an emergency department with that type of headache, subarachnoid hemorrhage turns out to be the cause in 11 to 25% of cases.
Aneurysms tend to form at branching points in arteries at the base of the brain, where blood flow creates extra stress on vessel walls. Over years, a combination of high blood pressure, inflammation, and genetic vulnerability can erode the wall until it gives way. Not every aneurysm ruptures, and size matters: larger aneurysms carry higher risk, though even small ones occasionally bleed.
Vascular Malformations
Brain arteriovenous malformations are tangles of abnormal blood vessels that connect arteries directly to veins, bypassing the normal capillary network. Because capillaries normally slow blood flow and reduce pressure, skipping them means the veins in the malformation handle far more pressure than they’re built for. This can lead to rupture, producing bleeding that may spill into brain tissue, the fluid-filled ventricles, the subarachnoid space, or all three at once.
These malformations are uncommon but disproportionately affect younger adults. Certain features raise the bleeding risk: aneurysms within the tangle itself, drainage into deep brain veins, blockages in the outflow veins, and location in deeper or lower parts of the brain. Between 15 and 30% of patients with these malformations also have associated aneurysms on the feeding arteries, which carry their own independent rupture risk.
High Blood Pressure
Chronic high blood pressure is one of the strongest modifiable risk factors for subarachnoid hemorrhage, and the relationship follows a clear staircase pattern. A large study published in the European Journal of Neurology tracked how risk climbed at each blood pressure threshold. Compared with people whose systolic pressure stayed below 120, those in the 120 to 130 range had a 41% higher risk. At 140 to 160, risk more than doubled. And people with readings above 180 faced nearly six times the risk.
High blood pressure damages artery walls over time, accelerating aneurysm formation and growth. It also increases the force acting on an existing aneurysm, making rupture more likely. Even a history of diagnosed hypertension, regardless of current readings, was associated with a 25% increase in subarachnoid hemorrhage risk.
Smoking
Smoking is the single most potent lifestyle risk factor. Current smokers face roughly three times the risk of never-smokers overall, but the numbers climb steeply with volume. People smoking up to a pack a day have about 2.8 times the risk, while those smoking more than a pack a day have 5.2 times the risk. Over a lifetime, accumulating 20 or more pack-years of smoking raises the risk fourfold.
The mechanism involves direct damage to blood vessel walls. Chemicals in cigarette smoke promote inflammation, break down structural proteins in artery walls, and interfere with the body’s ability to repair the damage. This weakens existing aneurysms and may contribute to forming new ones.
The good news is that the risk drops quickly after quitting. Former smokers, even those who were heavy smokers for years, show no statistically significant increase in risk compared to people who never smoked. Within a few years of quitting, the elevated risk is virtually eliminated. Roughly one in three cases of subarachnoid hemorrhage can be attributed to current smoking, making cessation one of the most effective preventive steps a person can take.
Cocaine and Other Stimulant Drugs
Cocaine triggers a sudden surge in blood pressure by flooding the brain with neurotransmitters and blocking their normal reabsorption. This acute spike can push an existing aneurysm past its breaking point. Repeated use also weakens blood vessel walls over time, potentially creating new aneurysms or making existing ones more fragile. Other stimulant drugs, including amphetamines, work through similar mechanisms and carry similar risks. The combination of chronic vessel damage and acute pressure spikes makes stimulant use a particularly dangerous trigger.
Genetic and Inherited Conditions
Some people are born with conditions that make their blood vessels more vulnerable. Autosomal dominant polycystic kidney disease, a genetic condition that causes cysts to grow in the kidneys, also affects blood vessel walls throughout the body. People with this condition develop brain aneurysms at three to five times the rate of the general population, with aneurysms found in 8 to 9% of affected individuals compared to 2 to 3% of the general population. For this reason, screening for brain aneurysms is often recommended for these patients.
Other connective tissue disorders that weaken blood vessel structure, such as Ehlers-Danlos syndrome and Marfan syndrome, also increase aneurysm risk. Having a first-degree relative who experienced a subarachnoid hemorrhage roughly doubles your own risk, even without a known genetic condition, suggesting that inherited variations in vessel wall strength play a role.
Why Women Face Higher Risk After Menopause
Women develop subarachnoid hemorrhage more often than men, and the gap widens significantly after menopause. The hormonal shift appears to be a key factor. A genetic study found that lower levels of bioavailable testosterone in women were associated with a 27% increase in subarachnoid hemorrhage risk. The relationship works through a binding protein that controls how much active testosterone circulates in the blood: higher levels of this protein (which reduce free testosterone) were linked to an 18% increase in risk per unit of change.
Testosterone and estrogen both have protective effects on blood vessel walls, helping to maintain flexibility and resist damage. When these hormones decline after menopause, vessel walls become more susceptible to the wear caused by high blood pressure and other stressors, accelerating aneurysm development.
Perimesencephalic Hemorrhage
In roughly 10 to 15% of non-traumatic cases, bleeding occurs in a specific pattern around the brainstem, and no aneurysm or malformation is found on imaging. This is called perimesencephalic subarachnoid hemorrhage, and it was first described as a distinct entity in 1985. The source of the bleeding is often never identified, though it likely originates from small veins rather than arteries.
This type is important to recognize because the outlook is dramatically better than for aneurysmal bleeding. People with perimesencephalic hemorrhage typically recover well, with low rates of the serious complications that make aneurysmal subarachnoid hemorrhage so dangerous, such as blood vessel spasm and recurrent bleeding.
How Multiple Risk Factors Interact
Subarachnoid hemorrhage rarely results from a single factor. A person might carry a small, stable aneurysm for decades without incident. But combine that aneurysm with uncontrolled blood pressure, heavy smoking, and a genetic predisposition to weak vessel walls, and the risk picture changes substantially. The modifiable risks, particularly smoking and blood pressure, are where prevention efforts have the most impact. Keeping blood pressure below 120 systolic and not smoking can meaningfully reduce the odds of a bleed, even in people with known aneurysms or a family history of hemorrhagic stroke.