A stroke is a race against tissue death. Every minute an ischaemic stroke goes untreated, an estimated 1.9 million neurons die. The imaging pathway that has been built around this fact is not accidental - CT first because it is fast and answers the one urgent question, MRI second because it answers the ten questions that decide what happens next. This guide walks through that sequence, what diffusion-weighted imaging actually shows, and why MRI matters even when the CT scan looks normal.
The one-line answer
In an acute suspected stroke, you get a CT scan within minutes. If the picture is right and the clock allows, you receive thrombolysis or thrombectomy immediately. MRI follows within hours or days to confirm the diagnosis on diffusion-weighted imaging, define the territory, and hunt for the cause. In a TIA, MRI is the first-line brain scan and should happen inside 24 hours.
Why CT is first in acute stroke
The acute stroke pathway is timed in minutes because the treatment windows are timed in minutes. Intravenous thrombolysis with alteplase or tenecteplase must be delivered inside 4.5 hours of symptom onset. Mechanical thrombectomy for a large-vessel occlusion is standard up to 6 hours, and up to 24 hours in carefully selected patients. Everything upstream of those treatments - assessment, scanning, decision - has to fit inside that window with time to spare.
CT wins the first slot for four hard reasons. It is fast, with a non-contrast head CT taking under five minutes from the moment the patient is on the table. It is available around the clock in every UK acute hospital that receives stroke calls. It reliably rules out intracranial haemorrhage, which is the one finding that absolutely forbids thrombolysis. And where CT angiography is added, it identifies the large-vessel occlusions that qualify a patient for thrombectomy and route them to a comprehensive stroke centre.
What CT is bad at in the first hours is showing the ischaemic stroke itself. In the first three to six hours, non-contrast CT is often normal or shows only subtle signs - loss of grey-white differentiation, sulcal effacement, a hyperdense middle cerebral artery. The absence of a visible infarct on CT does not mean there is no stroke. It usually means CT cannot see it yet.
What MRI adds: diffusion-weighted imaging
This is where diffusion-weighted imaging, or DWI, changes the picture. DWI is an MRI sequence that measures the microscopic random movement of water molecules inside brain tissue. In healthy brain, water diffuses freely. In an acutely ischaemic area, the sodium-potassium pumps at the cell membrane fail within minutes of the blood supply being cut off, water rushes into cells, and its normal diffusion becomes restricted. On the DWI image, that restricted diffusion shows up as an area of bright, hyperintense signal.
The clinical point is timing. DWI can detect an acute infarct within 10 to 30 minutes of onset, hours before CT will show anything. Modern brain MRI paired with the apparent diffusion coefficient (ADC) map is more than 95 per cent sensitive and specific for acute ischaemic stroke inside the first 24 hours. Nothing else in imaging comes close on that timescale.
DWI also answers questions that matter for management. It shows the exact territory of the infarct, distinguishes cortical from lacunar patterns, picks up multiple simultaneous infarcts that suggest an embolic source, and separates truly acute from older ischaemia. That last point is important - a patient with vague neurological symptoms and a normal-looking CT can turn out on DWI to have an acute infarct that needs urgent secondary prevention.
CT tells you whether you can treat. Diffusion-weighted MRI tells you what you are treating, where it is, and often why.
Perfusion MRI and thrombectomy selection
The extended-window thrombectomy revolution of the last decade rests on one imaging idea - the ischaemic penumbra. When a large artery is blocked, the core of the affected territory dies quickly. Around that core sits a rim of brain that is not yet dead but is under-perfused and will die without reperfusion. The bigger that rim relative to the core, the more brain there is to save, and the greater the argument for thrombectomy even hours after symptom onset.
MRI measures this directly. Perfusion-weighted imaging (PWI) shows the volume of brain that is not being perfused properly. DWI shows the volume that is already infarcted. The difference between the two - the DWI-PWI mismatch - is the penumbra. A large mismatch identifies patients who will benefit from thrombectomy up to 24 hours after onset, including wake-up strokes with an unknown time of onset. In centres without MRI, CT perfusion is used for the same purpose, but MRI-based selection is generally considered more precise.
TIA workup and MRI
A transient ischaemic attack is a stroke that got away with it. Symptoms resolve, usually within an hour, and by the time the patient is assessed the neurological examination is often normal. The temptation for both patient and clinician is to relax. This is a mistake. The 90-day stroke risk after a TIA is around 5 to 10 per cent, and much of that risk sits in the first 48 hours.
National Institute for Health and Care Excellence guidance is unambiguous: any suspected TIA should be assessed in a specialist clinic within 24 hours, with brain MRI including DWI as the first-line scan. The two questions MRI is answering here are different from the acute stroke pathway. First, has an actual infarct occurred, even though symptoms resolved? DWI will show it if it has, and that changes the diagnosis from TIA to minor ischaemic stroke, which changes the treatment. Second, what is the underlying vessel and cardiac territory pattern, so that the right secondary prevention starts immediately.
A proper TIA MRI is not just a brain scan. It includes magnetic resonance angiography (MRA) of the carotid and vertebral arteries, and often the intracranial circulation. Significant carotid stenosis identified on MRA needs urgent endarterectomy or stenting, ideally within two weeks. Missing it means the second event is more likely to be a completed stroke.
Post-stroke MRI for cause hunting
Once the acute phase is over, MRI does the detective work of secondary prevention. The pattern of infarcts on DWI is the first clue. Multiple bilateral infarcts in different vascular territories suggest a proximal embolic source - most commonly the heart or the aortic arch. A single deep lacunar infarct points to small vessel disease and blood pressure control. A cortical infarct in one territory raises the question of a carotid or intracranial artery lesion.
MRI also detects the causes that a routine workup would miss. Susceptibility-weighted imaging (SWI) picks up cerebral microbleeds and cortical superficial siderosis, both of which change the risk-benefit calculation for anticoagulation. Fat-suppressed neck MRI with T1 sequences is the standard for detecting arterial dissection in younger stroke patients. Where a patent foramen ovale (PFO) is suspected as a source of paradoxical embolism, the imaging picture on brain MRI - particularly the number and pattern of infarcts - feeds directly into the decision about closure.
