Stroke

TL;DR. A stroke is a heart attack of the brain. Either an artery is blocked (ischaemic, about 85 percent of cases) or one bursts (haemorrhagic, the rest). Brain tissue deprived of blood starts dying within minutes, at a rate of roughly 1.9 million neurons per minute, so every part of stroke care is organised around speed. Which abilities are lost (speech, movement, vision, balance, personality) depends entirely on which artery is involved, which is why two strokes can look like completely different diseases. Stroke is the second or third leading cause of death worldwide and the leading cause of acquired adult disability, and about 90 percent of the risk is attributable to factors that can be modified.

Key takeaways

• Almost 12 million strokes occur each year and over 7 million people die of one. Roughly 1 in 4 adults will have a stroke in their remaining lifetime after age 25.
• Time is brain. Treatments that dissolve or remove the clot work in hours, not days, and the benefit shrinks steeply with every minute of delay.
• FAST: Face drooping, Arm weakness, Speech difficulty, Time to call emergency services. Add BE for Balance and Eyes to catch posterior strokes.
• A transient ischaemic attack (TIA) is a stroke whose symptoms resolve. It is not a false alarm; it is a warning, with the highest risk of a full stroke in the following days.
• High blood pressure is the dominant risk factor for both types. The INTERSTROKE study found ten factors account for about 90 percent of stroke risk worldwide.
• Organised stroke unit care saves more lives at population level than any single drug, simply by doing the ordinary things (swallowing assessment, early mobilisation, clot prevention) reliably.

What it is

In short: Either a blocked artery or a burst one, and telling them apart needs a scan because the treatments are opposites.

The brain is about 2 percent of body weight and consumes roughly 20 percent of the body's oxygen. It stores almost no fuel, so it depends on continuous flow. Interrupt that flow and function stops within seconds and cells begin dying within minutes.

Ischaemic stroke (about 85 percent): an artery supplying part of the brain is blocked by a clot. The clot may form locally on an atherosclerotic plaque (Chapter 21), travel from the heart (usually from atrial fibrillation), or arise from small vessel disease deep in the brain.

Haemorrhagic stroke: a vessel ruptures and blood damages tissue directly, while also raising pressure inside the skull. Two subtypes: intracerebral haemorrhage (bleeding into brain tissue, usually from chronic hypertension) and subarachnoid haemorrhage (bleeding into the space around the brain, usually from a ruptured aneurysm, classically presenting as a "thunderclap" headache, the worst of the person's life, reaching maximum intensity within seconds).

Transient ischaemic attack: identical symptoms that resolve completely, usually within an hour, because the blockage clears itself. The risk of a full stroke in the following 90 days is substantial and is concentrated in the first two days, which makes a TIA an emergency, not a reassurance.

Don't be confused: the two stroke types need opposite treatments. An ischaemic stroke is treated by breaking up or removing a clot, using drugs that promote bleeding. Give those to someone with a brain haemorrhage and you will kill them. The two are indistinguishable at the bedside, which is why an urgent CT scan comes before any treatment. This is the entire reason stroke care requires a hospital rather than a paramedic's judgement.

The history

In short: CT scanning made diagnosis possible, thrombolysis made treatment possible, and five trials reported in 2015 made clot retrieval standard.

Apoplexy, from the Greek for "struck down," described sudden collapse and paralysis from antiquity. In 1658 Johann Jakob Wepfer performed autopsies showing bleeding into the brain in some cases and blocked vessels in others, distinguishing the two mechanisms for the first time. Rudolf Virchow in the mid-1800s described thrombosis and embolism and the conditions favouring clot formation still known as Virchow's triad.

For a century after that, diagnosis remained guesswork and treatment was supportive. Three developments made modern stroke care possible.

CT scanning, from the 1970s, allowed bleeding and blockage to be distinguished within minutes in a living patient. Everything downstream depends on this.

Thrombolysis. The NINDS trial in 1995 showed that intravenous alteplase, a clot-dissolving drug, given within three hours of symptom onset improved outcomes, despite causing some brain haemorrhages. The window was later extended to 4.5 hours.

Thrombectomy. In 2015, five randomised trials reported within months of each other (MR CLEAN, ESCAPE, EXTEND-IA, SWIFT PRIME, REVASCAT), all showing that physically retrieving a clot from a large artery with a catheter produced dramatically better outcomes than drugs alone. The effect size was among the largest in modern medicine: the number needed to treat for one patient to be functionally independent was in the range of 3 to 7. Trials in 2018 (DAWN, DEFUSE-3) extended the window to 24 hours in carefully selected patients using perfusion imaging to identify tissue still salvageable.

What actually goes wrong

In short: A dead core surrounded by a still-salvageable penumbra, which is what every acute stroke treatment is aimed at.

The ischaemic cascade

When flow stops, neurons run out of ATP within minutes. Without ATP the pumps that maintain ion gradients fail, sodium and calcium flood in, and the cell releases its stores of the neurotransmitter glutamate. Glutamate overstimulates neighbouring neurons, driving more calcium in, which activates enzymes that digest the cell from inside. This is excitotoxicity, and it spreads outward from the dead zone.

Two regions therefore exist:

• The core: flow near zero, cells dead within minutes, unsalvageable.
• The penumbra: surrounding tissue kept marginally alive by collateral vessels, electrically silent but structurally intact, and salvageable if flow is restored.

Every acute stroke treatment is aimed at the penumbra. Its size and how long it survives vary enormously between people, depending on their collateral circulation, which is why some patients benefit at 20 hours and others have lost everything at 3.

Where the clots come from

Why vessels burst

Intracerebral haemorrhage is overwhelmingly a consequence of chronic high blood pressure, which damages small deep arteries until they rupture. In older people, cerebral amyloid angiopathy (amyloid protein deposited in vessel walls, related to the protein in Alzheimer's disease) causes bleeding nearer the brain surface. Anticoagulant drugs increase the risk and worsen the outcome of any bleed.

Subarachnoid haemorrhage usually comes from a berry aneurysm, a balloon at an arterial branch point. Aneurysms are present in perhaps 3 percent of adults, and most never rupture. Risk of rupture rises with size, location, smoking, and hypertension.

What it does to the body

In short: The deficit maps precisely onto the artery involved, which is why two strokes can look like completely different diseases.

The lost function maps onto the damaged territory, which is why a neurologist can predict the artery from the deficit.

Longer-term consequences that are underappreciated: dysphagia (unsafe swallowing, leading to aspiration pneumonia, the leading cause of death in the weeks after a stroke), spasticity and contractures, post-stroke depression (affecting roughly a third), post-stroke fatigue, emotional lability, epilepsy in about 5 to 10 percent, and vascular cognitive impairment, which can progress to dementia.

Is it deadly?

• Nearly 12 million strokes and over 7 million stroke deaths annually. Stroke is the second leading cause of death worldwide and the third leading cause of death and disability combined.
• Roughly 1 in 4 people aged 25 and over will have a stroke in their remaining lifetime.
• About a third of survivors are left permanently dependent on others for daily activities, which makes stroke the leading cause of acquired adult disability.
• Haemorrhagic strokes are deadlier than ischaemic ones: intracerebral haemorrhage carries roughly 30 to 40 percent mortality at one month. Subarachnoid haemorrhage kills a substantial fraction before they reach hospital.
• The global burden is rising in absolute terms (ageing populations) while age-standardised rates fall in high-income countries, and over 85 percent of stroke deaths now occur in low- and middle-income countries.

Is it contagious?

No. A stroke is a vascular event in one person's brain.

Two indirect infection links exist. Acute infections, including influenza and COVID-19, transiently increase stroke risk in the following weeks through inflammation and clotting. And in children, some strokes follow varicella (chickenpox) infection causing inflammation of cerebral arteries. Neither makes stroke itself transmissible.

Who gets it

In short: Ten factors account for about 90 percent of stroke risk, with high blood pressure far ahead of everything else.

INTERSTROKE, a case-control study across 32 countries, found ten factors accounting for about 90 percent of population-attributable stroke risk: hypertension (the largest by a wide margin), physical inactivity, abnormal lipids, poor diet, abdominal obesity, psychosocial factors, smoking, cardiac causes (chiefly atrial fibrillation), alcohol, and diabetes.

Age roughly doubles risk every decade after 55, though about 10 to 15 percent of strokes occur in adults under 50, where dissection, patent foramen ovale, drug use, and clotting disorders are more prominent causes.

Sex. Men have more strokes at younger ages; women have more strokes overall because they live longer, and worse outcomes on average. Pregnancy, pre-eclampsia, and some hormonal contraception modestly raise risk.

Ancestry and geography. Stroke rates are highest in East Asia, Central and Eastern Europe, and parts of sub-Saharan Africa. In the United States and the UK, people of African and Caribbean descent have roughly twice the stroke rate of white populations at younger ages, tracking earlier and more severe hypertension. Intracranial atherosclerosis is a more common stroke mechanism in East Asian populations, while carotid disease is more common in European ones.

Specific high-risk groups: atrial fibrillation (a fivefold increase, largely preventable with anticoagulation), sickle cell disease (a major cause of childhood stroke, preventable by transcranial Doppler screening and transfusion), and people who have already had a TIA or stroke.

Treatment, and how it works

In short: Speed, then a scan, then drugs or clot retrieval, and then a stroke unit, which is the one intervention that benefits every patient.

The acute phase

1. Recognise and call. Symptom onset time is the single most important piece of information, because it determines eligibility for treatment. If onset was unwitnessed (waking with symptoms), imaging can sometimes estimate it.
2. Immediate CT. To exclude haemorrhage. CT angiography identifies large vessel occlusion; CT perfusion estimates core and penumbra.
3. Thrombolysis with alteplase or, increasingly, tenecteplase (a single bolus rather than an infusion, which is faster and more practical) within 4.5 hours. It activates plasminogen, dissolving the fibrin holding the clot together.
4. Mechanical thrombectomy for large vessel occlusion: a catheter is threaded from the groin or wrist into the cerebral artery and a stent-retriever or aspiration device pulls the clot out. Standard within 6 hours, and up to 24 hours in patients whose imaging shows salvageable tissue.
5. Stroke unit admission. Care in a dedicated unit with a specialist multidisciplinary team reduces death and dependency regardless of stroke type or treatment given. It remains the intervention that benefits the largest number of patients, because everyone is eligible.
6. Aspirin within 48 hours for ischaemic stroke; anticoagulation is generally delayed.
7. Decompressive hemicraniectomy (removing part of the skull to let a swelling brain expand) in selected younger patients with large strokes, which reduces mortality substantially at the cost of surviving with significant disability.

For haemorrhagic stroke: rapid blood pressure lowering, urgent reversal of any anticoagulant, neurosurgery in selected cases, and for a ruptured aneurysm, securing it by endovascular coiling (packing it with platinum coils via catheter) or surgical clipping.

Preventing the next one

• Antiplatelet therapy (aspirin, clopidogrel, or short-term dual therapy after minor stroke or high-risk TIA) for non-cardioembolic strokes.
• Anticoagulation for atrial fibrillation, which reduces stroke risk by about two-thirds and is the highest-yield preventive intervention in the field.
• Blood pressure lowering, the largest single lever.
• High-intensity statin, which reduces recurrent stroke and cardiac events.
• Carotid endarterectomy or stenting for significant symptomatic carotid narrowing, best done within two weeks of the event.
• Closure of a patent foramen ovale in selected young patients with otherwise unexplained stroke.

Rehabilitation

Recovery happens through neuroplasticity: surviving brain regions take over functions of the damaged area, and connections reorganise. This process is use-dependent, which is why rehabilitation is a treatment rather than a comfort. What the evidence supports: starting early (though not aggressively within the first 24 hours), high repetition and intensity, task-specific practice, and specialist speech and language therapy for aphasia and swallowing. Constraint-induced movement therapy, which restrains the good arm to force use of the affected one, has good evidence in selected patients. Most recovery occurs in the first three to six months, but improvement well beyond that is documented and the old teaching that recovery stops at six months is wrong.

What treatment costs

• Thrombolysis causes symptomatic intracranial haemorrhage in roughly 2 to 7 percent of treated patients, some fatal. It is given anyway because the net benefit across eligible patients is clearly positive, and this is a good example of a treatment whose harms are real, visible, and outweighed.
• Thrombectomy: vessel perforation, dissection, clot fragments travelling to new territories, groin haematoma. Complication rates are low in high-volume centres, which is an argument for centralised stroke services even at the cost of longer transport.
• Anticoagulants: bleeding, including the rare but serious intracranial bleed. The trade-off strongly favours treatment when atrial fibrillation stroke risk is meaningful.
• Decompressive surgery: survival with major disability is a realistic outcome, and the decision requires an honest conversation about what the patient would accept.

What the person can do

In short: Learn FAST, note the exact time symptoms began, and call an ambulance rather than driving to hospital.

Before a stroke, prevention is the same list as Chapter 20 and Chapter 21, with blood pressure at the top. Two additions specific to stroke: get an irregular pulse checked, because undiagnosed atrial fibrillation is common and silent, and take anticoagulation seriously if it is prescribed, because it is one of the most effective preventive drugs in medicine and adherence to it is poor.

During a stroke, the highest-value action belongs to whoever is nearby. Learn FAST. Note the time symptoms began. Call emergency services rather than a family doctor or a taxi, because ambulances pre-alert stroke teams and can route to a thrombectomy-capable centre. Do not give food, drink, or aspirin before assessment, since swallowing may be unsafe and the stroke may be a bleed.

After a stroke: attend rehabilitation and do the home exercises, which are the active ingredient; treat depression, which is common and undertreated and which impairs rehabilitation; take secondary prevention medication indefinitely; and address driving, work, and mood explicitly rather than waiting to be asked.

Living with it

Stroke is the most disability-producing common disease in this book, and much of the burden is invisible from outside. Aphasia is particularly isolating: intelligence and personality are intact while the ability to express them is not, and people frequently speak to a person with aphasia as though they were cognitively impaired. Neglect after a right-hemisphere stroke can be misread as inattention or lack of effort. Post-stroke fatigue is disproportionate to physical deficit and poorly understood.

Informal caregivers, usually family, provide most long-term care and experience high rates of depression and financial strain themselves. Caregiver support is part of stroke treatment rather than an optional extra.

What's next

• Mobile stroke units, ambulances carrying a CT scanner, delivering thrombolysis at the roadside and cutting time to treatment substantially.
• Tenecteplase replacing alteplase as the standard thrombolytic on practical grounds.
• AI imaging triage, automatically detecting large vessel occlusion on CT and alerting the thrombectomy team while the patient is still in the scanner.
• Extended and imaging-selected windows, moving from clock-based to tissue-based eligibility.
• Neuroprotection, a field with a long record of failure in humans despite success in animals, now being retried in combination with reperfusion rather than instead of it.
• Wider access. The largest available gain worldwide is not a new drug; it is organised stroke units and basic hypertension control in the countries where 85 percent of stroke deaths now occur.

Sources and notes

Incidence, mortality, and lifetime risk figures are from the World Stroke Organization Global Stroke Fact Sheet 2025 and Global Burden of Disease analyses: nearly 12 million new strokes and over 7 million deaths annually, and approximately 1 in 4 lifetime risk after age 25. The 1.9 million neurons per minute estimate is from Saver, Stroke, 2006. INTERSTROKE: O'Donnell et al., The Lancet, 2010 and 2016. NINDS alteplase trial: NEJM, 1995. The 2015 thrombectomy trials: MR CLEAN, ESCAPE, EXTEND-IA, SWIFT PRIME, REVASCAT, with the HERMES pooled analysis. Extended window: DAWN and DEFUSE-3, NEJM, 2018. Stroke unit care: Stroke Unit Trialists' Collaboration, Cochrane reviews. Subtype proportions follow TOAST classification studies and vary by population.

Open questions. Whether thrombectomy benefits patients with large established cores is being actively redefined by recent trials. Optimal blood pressure targets in the first days after ischaemic stroke remain uncertain. No neuroprotective agent has yet succeeded in humans.

Next: the organ that quietly cleans everything up, and what happens when it stops. 👉