18.6 — Stroke

Around 1.9 million neurons die every minute during a large vessel stroke.

"Time is brain" is the phrase, and the arithmetic behind it is stark: each hour of delay ages the affected brain by around 3.6 years.

Which makes stroke, more than almost any condition in this volume, a disease where the outcome is determined by how fast someone recognises it and calls for help.

The two kinds

Ischaemic — around 85 percent. A vessel is blocked.

Haemorrhagic — around 15 percent. A vessel bursts.

And they cannot be distinguished clinically. The symptoms are identical, and the treatments are opposite — one needs the clot dissolved or removed, the other would be made catastrophically worse by that.

Which is why the first test in every stroke is a brain scan, and why nothing that thins the blood is given until it is done.

Causes of ischaemic stroke:

Large artery atherosclerosis — usually the carotid. Cardioembolic — a clot from the heart, most often from atrial fibrillation (Chapter 18.5). Small vessel disease — the deep perforating arteries, driven mainly by hypertension and diabetes, producing lacunar strokes. And in younger people: arterial dissection, patent foramen ovale (Chapter 7.9), clotting disorders, and vasculitis.

Causes of haemorrhagic stroke:

Hypertension — the dominant cause of deep intracerebral haemorrhage. Cerebral amyloid angiopathy — in older people, causing lobar bleeds. Aneurysm rupture — subarachnoid haemorrhage (Chapter 11.10). Vascular malformations, and anticoagulation.

Recognising it

And this is the section that matters most.

FAST:

F — Face. Has their face fallen on one side? Can they smile? A — Arms. Can they raise both arms and keep them there? S — Speech. Is it slurred? Can they understand you? T — Time. Call an ambulance immediately.

FAST detects around 80 to 90 percent of strokes, and it is deliberately simple because it has to work for a frightened bystander.

What it misses, and these matter:

Sudden severe dizziness with inability to walk — posterior circulation stroke (Chapter 11.12). The discriminator is that someone with a benign inner ear problem can usually walk unsteadily; someone with a cerebellar stroke frequently cannot stand at all.

Sudden visual loss or double vision.

Sudden severe headache — particularly if it reaches maximum intensity within seconds, which is subarachnoid haemorrhage (Chapter 11.10).

Sudden confusion.

Which is why the extended version — BE-FAST — adds Balance and Eyes.

And one distinction is worth carrying (Chapter 6.3): a stroke affecting the face spares the forehead, because the forehead has bilateral cortical supply. A person who cannot smile on one side but can still raise both eyebrows has had a stroke; one who cannot move the forehead either has a facial nerve palsy. Three seconds, and it separates an emergency from a benign condition.

What to do

Call an ambulance. Note the time symptoms started — or the time the person was last seen well, if they woke with them.

That time determines everything about the treatment, and it is the single most useful piece of information a bystander can provide.

Do not give aspirin — because a haemorrhage has not been excluded.

Do not give food or drink — swallowing is frequently impaired.

Lie them down with the head slightly raised, and stay with them.

Treatment

Thrombolysis — clot-busting drugs, within 4.5 hours of onset, and the benefit falls sharply with every minute.

Around 1 in 3 treated patients has a better outcome than they would have had, and around 1 in 20 to 30 suffers a symptomatic bleed.

Thrombectomy — mechanically retrieving the clot through a catheter, for large vessel occlusions.

And this is the largest advance in stroke care in decades. The trials published from 2015 onward showed effect sizes rarely seen in medicine — a number needed to treat of around 3 to 5 for improved functional outcome.

The window extends to 6 hours routinely, and up to 24 hours in selected patients where advanced imaging shows brain tissue that is still salvageable — which is a genuine shift from a fixed time window to a physiological one.

It requires a specialist centre, which is why ambulance protocols now bypass local hospitals to reach one.

For haemorrhagic stroke: reversing anticoagulation urgently, controlling blood pressure, and neurosurgery in selected cases.

Stroke units — and this deserves emphasis because it is unglamorous and highly effective.

Being cared for on a dedicated stroke unit reduces death and dependency by around 20 percent, independent of any specific treatment. The mechanism is coordinated multidisciplinary care: early swallow assessment, early mobilisation, prevention of complications, and rehabilitation started immediately.

The aftermath

And the range of consequences reflects the map in Chapter 11.5.

Weakness on the opposite side, because the motor tracts cross (Chapter 11.3).

Aphasia — from dominant hemisphere damage. Expressive (Broca's): knows what to say, cannot produce it, and is acutely aware and frustrated. Receptive (Wernicke's): fluent, meaningless speech, impaired comprehension, and often unaware of the problem.

Neglect — from non-dominant parietal damage. Not attending to one side of space or of the body, and frequently denying anything is wrong. It is a major obstacle to rehabilitation and is frequently mistaken for confusion or non-cooperation.

Swallowing difficulty — affecting around half acutely. Aspiration pneumonia is a leading cause of death after stroke, which is why nothing is given by mouth until swallowing is assessed (Chapter 6.3).

Visual field loss — and the person may not be aware of it, which matters for driving.

Emotional lability — sudden uncontrollable crying or laughing disconnected from mood (Chapter 11.7). Distressing, frequently misinterpreted as depression, and treatable.

Post-stroke depression — affecting around a third, associated with worse recovery, and under-treated.

Fatigue — extremely common, persistent, and consistently underestimated by everyone except the patient.

Central post-stroke pain — burning pain in the affected area, from thalamic damage (Chapter 11.4). Difficult to treat.

Recovery

And the outlook is better than it is usually presented.

Recovery comes from three sources: resolution of swelling around the damaged area in the first weeks; surviving pathways taking over function; and learned compensation (Chapter 11.5).

The old teaching that recovery plateaus at six months has been substantially revised. Improvement continues for years with appropriate training, and intensity of therapy matters more than its timing.

Constraint-induced movement therapy — restraining the good arm to force use of the affected one — produces measurable functional gains and cortical reorganisation, including years after the stroke.

Early mobilisation improves outcomes, though very early aggressive mobilisation within 24 hours was found in one large trial to be worse — so the current position is early but graded.

And rehabilitation is the intervention with the largest effect on final function, which makes access to it the main determinant of long-term outcome in most health systems.

TIA — the warning

A transient ischaemic attack: stroke symptoms resolving completely, usually within an hour.

And it is a medical emergency rather than a reassuring event.

The risk of a full stroke after a TIA is around 5 percent within 48 hours and up to 10 percent within a week — and it is highest in the first two days.

Which means "it went away" is exactly the wrong conclusion.

Urgent assessment — within 24 hours — plus immediate antiplatelet treatment reduces subsequent stroke risk by around 80 percent.

That figure comes from studies comparing rapid-access clinics with routine referral, and it is one of the largest effects available from simply doing something quickly.

Anyone with transient weakness, speech disturbance or visual loss should be assessed the same day, whether or not it has resolved.

Prevention

Around 90 percent of stroke risk is attributable to modifiable factors, from the INTERSTROKE study — the same finding as for heart attack (Chapter 18.1).

Blood pressure is the largest single one. Controlling it is the highest-yield stroke prevention there is (Chapter 18.2).

Atrial fibrillation — detection and anticoagulation (Chapter 18.5).

Smoking, diabetes, cholesterol, physical inactivity, diet, obesity, alcohol, and psychosocial stress.

Carotid stenosis — surgery or stenting for severe narrowing, particularly after a TIA or minor stroke on that side.

And secondary prevention after a stroke: antiplatelet or anticoagulant depending on the cause, a statin, blood pressure control, and addressing the specific mechanism.

The direction of travel

Stroke mortality has fallen substantially in most high-income countries over the past few decades — from better blood pressure control, smoking reduction, stroke units, and now thrombectomy.

And thrombectomy in particular changed something fundamental: a large vessel stroke, previously the worst kind, became the one most amenable to treatment.

The limiting factor is now recognition and transport. Which puts a substantial part of the outcome in the hands of whoever is present when it happens — and is why FAST is worth knowing by heart.

What the next page fixes

Chapter 18.7 covers the condition that raises the risk of everything in this Part, affects over 500 million people, and — in its commonest form — can be pushed into remission.