A stroke happens when blood flow to part of the brain is suddenly cut off, either by a blockage in a blood vessel or by a vessel bursting and bleeding into the brain. Without that blood supply, brain cells begin dying fast. Research published in the journal Stroke found that every minute a large-vessel stroke goes untreated, the average patient loses 1.9 million neurons, 13.8 billion synapses, and 7.5 miles of nerve fibers. In 2021 alone, there were 11.9 million new stroke cases worldwide.
The two broad categories, blocked vessels and burst vessels, account for every stroke. But within those categories, the specific ways a stroke can start vary widely, from a clot forming in the heart to a torn artery in the neck to a tiny balloon-like weak spot in the brain that finally gives way.
Blocked Blood Flow: Ischemic Stroke
Roughly 85% of all strokes are ischemic, meaning something blocks an artery supplying the brain. The three recognized mechanisms are embolism (a clot that travels), thrombosis (a clot that forms in place), and decreased perfusion (an overall drop in blood flow). In practice, embolism and thrombosis cause the vast majority.
Clots That Travel From Somewhere Else
An embolism happens when a blood clot forms in one part of the body, breaks free, and travels through the bloodstream until it lodges in a brain artery too narrow to let it pass. The clot can originate in two places: the heart or a large artery leading to the brain.
Heart-related clots are most commonly linked to atrial fibrillation, an irregular heart rhythm affecting millions of people. When the upper chambers of the heart quiver instead of contracting normally, blood pools and sits still in a small pouch called the left atrial appendage. That stagnant blood is prone to clotting. If a clot forms and gets pumped out, it can travel straight up to the brain. This process, blood sitting still and then clotting, follows a principle cardiologists have recognized for over a century.
Clots can also break off from fatty plaque deposits lining the carotid arteries in the neck. These artery-to-artery clots are considered the most common cause of stroke linked to large-artery disease. Plaque builds up over years, narrows the vessel, and pieces of it (or clots that form on its rough surface) can dislodge and shoot upstream into the brain.
Clots That Form in Place
Thrombosis means a clot builds up right where it causes the blockage. This can happen in large arteries, but it’s especially important in the tiny arteries deep inside the brain. These small, deep blockages produce what doctors call lacunar infarcts, small cavities of dead tissue caused by the closure of very narrow penetrating arteries.
Chronic high blood pressure is the main driver here. Years of elevated pressure damages the walls of these tiny vessels, causing them to thicken, stiffen, and eventually close off. In people with hypertension, the smallest arteries (under a fifth of a millimeter wide) can degenerate to the point of shutting down entirely. The resulting strokes tend to be smaller than those caused by large-artery blockages, but they can still cause significant disability depending on their location.
Burst Blood Vessels: Hemorrhagic Stroke
Hemorrhagic strokes are less common but more deadly. They happen when a blood vessel in or around the brain ruptures, flooding surrounding tissue with blood. The leaked blood puts pressure on brain cells and cuts off the normal blood supply downstream.
The two main types are intracerebral hemorrhage, where bleeding occurs inside the brain itself, and subarachnoid hemorrhage, where bleeding happens in the space between the brain and the thin layers of tissue covering it.
The most common causes of vessel rupture are aneurysms and arteriovenous malformations. An aneurysm is a weak spot in an artery wall that balloons outward over time. If it bursts, blood pours into the brain or the surrounding space. Subarachnoid hemorrhages are often triggered this way, when an aneurysm on the brain’s surface gives way. An arteriovenous malformation (AVM) is a tangled knot of abnormal blood vessels where arteries connect directly to veins without the normal network of tiny capillaries in between. These tangles have thinner, weaker walls than normal vessels and can rupture under pressure.
Uncontrolled high blood pressure is also a major contributor. Over time, it weakens small arteries deep in the brain, and a sudden spike can cause one to burst. This is the most frequent cause of intracerebral hemorrhage in older adults.
Strokes With No Obvious Cause
In a significant number of cases, particularly in younger patients, no clear source of a stroke can be identified even after thorough testing. These are called cryptogenic strokes. One increasingly recognized explanation is a patent foramen ovale (PFO), a small hole between the two upper chambers of the heart that normally closes shortly after birth but remains open in roughly a quarter of the population.
Most people with a PFO never have problems. But if a blood clot forms in a vein (say, in the legs), it can pass through the hole, bypass the lungs where it would normally get filtered out, and travel directly to the brain. Research in the Journal of the American Heart Association estimates that roughly 60% of cryptogenic ischemic strokes in young adults can be attributed to a PFO, making it a surprisingly common hidden contributor.
Torn Arteries in Younger Adults
Stroke in people under 50 often has different causes than stroke in older adults. One of the most important is cervical artery dissection, a tear in the inner wall of a major artery in the neck. This contributes to about 2% of all ischemic strokes but up to 25% of strokes in adults younger than 50.
The tear doesn’t require a major injury. It can happen during sports, chiropractic manipulation, or even seemingly minor neck movements. Once the inner wall tears, blood seeps between the layers of the artery wall, causing it to swell inward and narrow the channel. A clot can form at the site of the tear and either block the artery directly or break off and travel to the brain. The underlying causes are varied: connective tissue disorders, unusual anatomy in the neck, or sometimes no identifiable trigger at all.
Warning Strokes: Transient Ischemic Attacks
A transient ischemic attack (TIA) involves the same mechanisms as a full ischemic stroke, a temporary blockage of blood flow to the brain, but without lasting tissue damage. You might experience sudden numbness, trouble speaking, or vision loss that resolves within minutes to hours. The old definition set a 24-hour cutoff, but that’s been abandoned. What distinguishes a TIA from a stroke is whether brain tissue was actually destroyed, which can only be confirmed through imaging.
A TIA is not a mild event to brush off. It signals that the same process that causes a full stroke is actively underway. The same plaque, the same clot-forming conditions, or the same heart rhythm problem that produced the temporary blockage can produce a permanent one. Neuroimaging, preferably an MRI, is recommended within 24 hours of symptoms to determine whether the event was truly a TIA or a stroke that happened to produce subtle symptoms.
How Multiple Risk Factors Compound
Most strokes don’t result from a single problem acting alone. High blood pressure damages vessel walls, making them more susceptible to both clots and rupture. Diabetes accelerates plaque buildup. Atrial fibrillation creates the stagnant blood conditions that generate clots. Smoking stiffens arteries and promotes inflammation. High cholesterol feeds the plaque deposits in the carotid arteries that shed clot fragments.
These factors layer on top of each other. Someone with both high blood pressure and atrial fibrillation faces a far higher stroke risk than someone with either condition alone. The common thread across nearly every stroke mechanism is damage to blood vessel walls, abnormal blood flow, or blood that clots too easily. Most of the time, the process builds silently over years before a stroke finally happens in seconds.