Strokes happen when blood flow to part of the brain is cut off, either by a blockage or by bleeding from a ruptured blood vessel. The causes range from conditions you may already know about, like high blood pressure and irregular heartbeat, to less obvious triggers like sleep apnea and tears in neck arteries. Understanding what drives each type helps you recognize which risks apply to you.
Two Types, Two Mechanisms
About 87% of strokes are ischemic, meaning a clot blocks blood flow to the brain. The remaining cases are hemorrhagic, caused by a blood vessel bursting and bleeding into or around brain tissue. The causes behind each type overlap in some areas and diverge sharply in others.
In ischemic stroke, the clot forms in one of two ways. A thrombotic stroke happens when a clot develops directly inside a brain artery, usually at a spot narrowed by fatty plaque buildup. An embolic stroke happens when a clot forms somewhere else in the body, typically the heart or a large neck artery, breaks loose, and travels to the brain. The distinction matters because the underlying cause you need to address is different in each case.
High Blood Pressure
High blood pressure is the single largest risk factor for both ischemic and hemorrhagic stroke. Stroke risk rises continuously once blood pressure exceeds about 115/75 mmHg, with no safe threshold below which lower pressure stops being beneficial. Each 10 mmHg drop in systolic pressure (the top number) is associated with roughly a one-third reduction in stroke risk for people in their 60s and 70s. For people under 60, the benefit is even larger, closer to 40% to 50% lower risk per 10 mmHg reduction.
In hemorrhagic stroke specifically, sustained high blood pressure weakens small arteries deep in the brain. Over time, the constant force damages vessel walls until one eventually ruptures and bleeds into surrounding tissue. This is the most common cause of the type of hemorrhagic stroke called intracerebral hemorrhage.
Atrial Fibrillation and Heart-Related Causes
Atrial fibrillation, an irregular and often rapid heartbeat, is one of the most significant causes of embolic stroke. When the heart’s upper chambers quiver instead of contracting properly, blood pools and can form clots. Those clots then travel through the arteries to the brain. The annual stroke risk for someone with atrial fibrillation ranges from about 1% to over 18%, depending on other factors like age, history of prior stroke, diabetes, and heart failure.
Other heart conditions can also send clots to the brain. Damaged or artificial heart valves, recent heart attacks that leave weakened heart muscle, and a hole between the heart’s upper chambers (called a patent foramen ovale) can all allow clots to reach the brain’s blood supply. Heart-related clots tend to cause larger strokes because they often block major arteries.
Atherosclerosis and Plaque Buildup
Atherosclerosis, the gradual buildup of fatty deposits inside artery walls, is the most common underlying process behind thrombotic strokes. Plaque narrows the artery over years, reducing blood flow. But the acute danger comes when a plaque ruptures. The body treats the exposed plaque like a wound, triggering clot formation at the site, which can seal off the artery entirely.
The carotid arteries in the neck are a particularly important location. Plaque here can cause stroke in two ways: by narrowing the artery enough to starve the brain of blood, or by sending fragments of clot downstream into smaller brain arteries. This artery-to-artery embolism is a common stroke mechanism, especially in older adults with significant vascular disease.
Diabetes
Diabetes accelerates nearly every vascular process that leads to stroke. Chronically elevated blood sugar damages the inner lining of blood vessels, impairing their ability to dilate and regulate blood flow. It increases arterial stiffness at younger ages, promotes system-wide inflammation, and thickens the walls of the smallest blood vessels. People with diabetes also show increased platelet stickiness during an acute stroke, which can worsen the clotting process.
These changes add up to faster, more aggressive plaque buildup in both the large arteries supplying the brain and the small vessels within it. Type 1 diabetes is particularly associated with early structural changes in the carotid artery wall, a recognized early sign of atherosclerosis.
Smoking
Current smokers face at least two to four times the stroke risk of people who have never smoked. The risk scales with how much you smoke. Women smoking 15 or more cigarettes per day have roughly triple the risk of hemorrhagic stroke compared to nonsmokers. For men smoking 20 or more per day, the risk of bleeding around the brain is about three times higher as well.
Smoking damages blood vessel walls, promotes clot formation, accelerates plaque buildup, and raises blood pressure. The encouraging finding is that quitting substantially reduces risk. People who stopped smoking more than 10 years ago have stroke risk comparable to those who never smoked.
Aneurysms and Blood Vessel Malformations
Hemorrhagic strokes have a distinct set of structural causes beyond high blood pressure. A cerebral aneurysm is a weak spot on a brain artery wall, typically where the artery branches. Blood pressure pushes against this weak point, forming a balloon-like bulge. As the aneurysm grows, its walls thin until they eventually burst, causing sudden bleeding around the brain (subarachnoid hemorrhage). Many people live with small aneurysms without knowing it until one ruptures.
Arteriovenous malformations are abnormal tangles of blood vessels in the brain where arteries connect directly to veins, bypassing the normal capillary network. These tangles disrupt normal blood flow and can rupture. They’re less common than aneurysms but are a recognized cause of hemorrhagic stroke, particularly in younger adults.
Sleep Apnea
Obstructive sleep apnea, where breathing repeatedly stops during sleep, is an underrecognized stroke risk factor. Each time breathing pauses, blood oxygen levels drop. This triggers a cascade of problems: the nervous system floods the body with stress hormones, inflammatory chemicals damage blood vessel walls, platelets become stickier and more prone to clotting, and oxidative stress accumulates in brain tissue.
The severity of the risk tracks with the severity of the sleep apnea. When oxygen saturation drops below 90% and breathing interruptions are frequent (15 or more per hour), the damage to blood vessels and brain tissue becomes more pronounced. Chronic oxygen deprivation without adequate recovery between episodes leads to ongoing vascular injury that can ultimately cause a stroke or transient ischemic attack.
Neck Artery Dissection in Younger Adults
Stroke in people under 50 often has different causes than in older adults. The most common distinct cause is cervical artery dissection, a tear in the inner wall of one of the arteries running through the neck to the brain. This tear allows blood to collect between the layers of the artery wall, narrowing the vessel and creating an environment where clots form. Those clots can then break off and travel to the brain.
Cervical artery dissection accounts for roughly 13% to 20% of ischemic strokes in adults aged 18 to 45, compared to just 2.5% of strokes in the general population. It can happen after neck trauma, chiropractic manipulation, or vigorous physical activity, though it sometimes occurs without any identifiable trigger. In people under 25 who have a stroke, dissection is the cause in up to 20% of cases.
Transient Ischemic Attacks as a Warning
A transient ischemic attack, often called a mini-stroke, produces stroke symptoms that resolve on their own, usually within minutes to hours. The temporary nature can be misleading. A TIA signals that the conditions for a full stroke are already in place. In one study tracking patients after a TIA, about 22% of subsequent strokes occurred within the first week, and 31% within 30 days. Nearly half of all strokes that followed a TIA happened within the first year.
A TIA is not a minor event. It’s a direct warning that one of the mechanisms described above, whether plaque rupture, a cardiac clot source, or arterial narrowing, is actively threatening your brain. The days and weeks immediately following a TIA represent the highest-risk window for a full stroke.