After a stroke, "the tests" means three different things: the bloods on the first day that decide the acute treatment; the tests over the following weeks that find the cause; and the extended blood, genetic and heart tests for strokes that are young, unexplained or unusual. This chapter lists all three, what each one is for, and what a result changes. The imaging and rhythm monitoring are in the cause chapter; this is the blood and genetic side, with the heart tests summarised.
1. Tier one: the first 24 hours, everyone
| Test | Why | What an abnormal result changes |
|---|---|---|
| Finger-prick glucose, then laboratory glucose | Low sugar mimics a stroke; high sugar worsens one | Corrected before any other decision |
| Full blood count | Platelets before thrombolysis; anaemia; polycythaemia | Platelets under 100 bar thrombolysis. A high haemoglobin or platelet count is a myeloproliferative clue (tier three) |
| Clotting screen (INR, APTT), and a DOAC level if the person takes one | Thrombolysis eligibility; reversal decisions in haemorrhage | INR over 1.7, or a DOAC within 48 hours without a drug-specific assay showing low levels, bars thrombolysis; for a bleed, decides the reversal agent |
| Kidney function, electrolytes | Contrast for CT angiography; drug dosing | Contrast is not withheld for an emergency angiogram; later, decides DOAC doses |
| Liver function | Baseline; statin and anticoagulant safety | Rarely changes the acute plan |
| Troponin | A heart attack can cause or accompany a stroke; recommended by the 2026 US guideline | A raised level means an ECG review and cardiology input; the stroke is still treated first |
| Lipid profile (total, LDL, HDL, non-HDL, triglycerides) | Baseline for the target in the prevention chapter | Valid without fasting and within 24–48 hours; after that the acute illness lowers it. Everyone starts a high-intensity statin regardless |
| HbA1c | Undiagnosed diabetes is common after a stroke | 48 or more is diabetes; 42–47 prediabetes; both change the long-term plan |
| CRP and ESR | Infection, endocarditis, vasculitis, giant cell arteritis | A high level with fever prompts blood cultures and an echocardiogram for endocarditis; in someone over 50 with headache or jaw pain, an urgent giant cell arteritis pathway |
| ECG, then continuous monitoring | Atrial fibrillation; a recent heart attack | AF changes the antithrombotic from antiplatelet to anticoagulant |
| Pregnancy test | Anyone who could be pregnant | Changes imaging choices and drugs; pregnancy and the weeks after are a stroke risk period |
| Blood cultures | If febrile, a murmur, injecting drug use, or a prosthetic valve | Endocarditis changes everything: no thrombolysis, no anticoagulation, antibiotics and surgery |
| Toxicology screen | Younger people; an unexplained stroke | Cocaine and amphetamines cause strokes and change the advice |
| Thyroid function | If atrial fibrillation is found | Thyrotoxicosis is a reversible cause of AF |
2. Tier two: the cause-finding weeks
- Lipoprotein(a), once in a lifetime: an inherited particle that raises stroke and heart-attack risk and is not lowered by statins. A high level changes how aggressively the other lipids are treated, prompts testing of first-degree relatives, and may open access to specific drugs as they arrive. Both UK and US lipid guidance now recommend measuring it once in anyone with premature or unexplained vascular disease.
- Repeat lipids on treatment at four to twelve weeks against the LDL target of 1.8 mmol/L, and the treatment stepped up if it is not met. This is the test most often not done.
- Kidney function repeated after any new blood-pressure drug or DOAC.
- Syphilis serology and HIV in younger or unexplained strokes: both are treatable causes of stroke and both are missed when nobody thinks to ask.
- Heart tests: an echocardiogram in everyone (clot in the heart, valve disease, a weak ventricle, an enlarged atrium); a bubble study in anyone under 60 with no other cause (a patent foramen ovale); a transoesophageal echo where the transthoracic one is inconclusive; and prolonged rhythm monitoring with a wearable or an implanted recorder if no cause has been found (the cause chapter).
- Carotid and intracranial imaging if not already done at the first scan; and MRI of the brain where the CT was unclear or the stroke was small or posterior.
3. Tier three: young, unexplained or unusual strokes
Justified by a stroke under 50 to 55, a stroke with no cause found after tiers one and two, strokes in several territories, strokes with systemic symptoms, a family history of early strokes or dementia, or a bleed with no hypertension. Ordered through a stroke or neurology clinic with haematology, rheumatology or genetics input as needed.
| Test | Looks for | Clue that justifies it | What a positive changes |
|---|---|---|---|
| Antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, anti-β2-glycoprotein I; repeated at 12 weeks) | Antiphospholipid syndrome, which causes arterial as well as venous clots | Any young or unexplained stroke; previous clots or miscarriages; low platelets; lupus | Warfarin rather than antiplatelets or a DOAC, long term; rheumatology input; pregnancy planning |
| Autoimmune and vasculitis screen (ANA, anti-dsDNA, ENA, ANCA, complement, ESR) | Lupus, systemic vasculitis, other connective tissue disease | Rash, joint pain, mouth ulcers, fever, weight loss, multiple small strokes, raised inflammatory markers | Immunosuppression treats the cause; vessel-wall MRI, CSF examination or biopsy may follow for suspected cerebral vasculitis |
| Haemoglobin electrophoresis | Sickle cell disease or trait | African or Caribbean heritage without a known diagnosis; any child | A transfusion programme and specialist care |
| JAK2 V617F (then CALR, MPL) | A myeloproliferative neoplasm | A raised haemoglobin, haematocrit or platelet count | Haematology diagnosis; venesection or cytoreduction reduces stroke risk |
| Protein electrophoresis, plasma viscosity | Myeloma, Waldenström's and hyperviscosity | Older person with anaemia, high ESR, bone pain, high calcium | Haematology diagnosis |
| Homocysteine | Homocystinuria (rare, inherited) and severe B12 or folate deficiency | Stroke under 40, tall thin build, dislocated lenses, learning difficulty; or a very low B12. Not as a routine risk marker: lowering a mildly raised level does not prevent stroke | Metabolic referral; specific diet and vitamins; B12 replacement |
| Fabry disease (alpha-galactosidase A activity in men; GLA gene and lyso-Gb3 in women) | An inherited enzyme deficiency that causes strokes, kidney disease and heart thickening | Unexplained stroke under 55; burning pain in hands and feet since childhood; skin angiokeratomas; kidney disease; a thick heart on echo; a family pattern. Found in around 1% of unexplained young strokes | Enzyme replacement or chaperone therapy; family cascade testing |
| NOTCH3 gene (CADASIL) | The commonest inherited small-vessel disease | Migraine with aura, strokes and early dementia in the family; the characteristic MRI pattern in the temporal poles and external capsules | No specific treatment, but it changes the prognosis, the risk-factor targets, the advice to avoid thrombolysis in some centres, and family counselling. NCGS 2023 has a dedicated section |
| Other monogenic small-vessel and stroke genes: HTRA1 (CARASIL), COL4A1/COL4A2 (bleeds and porencephaly), RNF213 (moyamoya, mainly East Asian ancestry), the mitochondrial m.3243A>G variant (MELAS: stroke-like episodes that do not follow an artery, with lactate raised) | Rare inherited stroke syndromes | A specific phenotype or family pattern, assessed by a neurologist or geneticist; usually as part of a panel once CADASIL is negative | Prognosis and family counselling; MELAS has its own metabolic management |
| Inherited thrombophilia (factor V Leiden, prothrombin G20210A, protein C, protein S, antithrombin) | Venous clotting tendency | Only when a venous route to the brain is plausible: a patent foramen ovale with a leg or pelvic clot, or a cerebral venous thrombosis. Not for an ordinary arterial stroke, where these variants are not a cause | Rarely anything on its own; informs the PFO closure and anticoagulation discussion. The full list is in the PE topic's every-test chapter |
| Cancer-directed tests | An occult cancer causing clots in several territories | Weight loss, a very high D-dimer, strokes in more than one arterial territory with no heart source, a history of cancer | The suspected-cancer pathway; anticoagulation rather than antiplatelets while the cancer is active |
| Cerebrospinal fluid | Infection or inflammation of the arteries or meninges | Fever, headache, raised inflammatory markers, an immunosuppressed person | Antimicrobials or immunosuppression |
| Temporal artery ultrasound or biopsy | Giant cell arteritis | Over 50 with headache, jaw pain, scalp tenderness, a high ESR, visual symptoms | High-dose steroids at once; a treatable cause of stroke and blindness |
| Neck artery imaging with fat-suppressed MRI | Arterial dissection | Neck pain or headache before the stroke; neck trauma or manipulation; a drooping eyelid; under 50 | Three to six months of an antithrombotic, then usually stop |
4. After a bleed
The tier-one clotting screen with fibrinogen and platelets, plus a DOAC level, decides reversal. Liver function and alcohol history matter more than in an ischaemic stroke. There is no blood test for cerebral amyloid angiopathy, the commonest cause of lobar bleeds in older people; it is an MRI diagnosis, and APOE genotyping, although associated, is not used clinically. A bleed in a younger person without hypertension needs vascular imaging for an aneurysm or a malformation, and a repeat MRI at two to three months once the blood has cleared, to look for a tumour or a cavernoma. A family history of bleeds prompts consideration of the COL4A1/A2 and cavernoma genes.
5. Tests that are sold but not worth doing
- MTHFR: no clinically significant link to stroke, and not recommended by any guideline.
- A "thrombophilia screen" for an ordinary arterial stroke: the venous variants do not cause arterial strokes, and the results change nothing.
- Homocysteine as a routine risk marker, and vitamin treatment to lower it: the trials found no stroke reduction.
- Broad "stroke gene panels" without a phenotype: they generate variants of uncertain significance and anxiety; genetic testing follows a clinical or family clue.
- Repeated lipoprotein(a): it is genetic and barely changes; once is enough.
- Routine CT of the body for cancer after a stroke: directed by symptoms only, as after a clot.
6. The list, in one paragraph, for the clinic
"Were my lipids and HbA1c measured, and has the LDL been rechecked on treatment against 1.8?" "Has lipoprotein(a) been measured once?" "Has my heart been monitored for long enough to find atrial fibrillation, and was a bubble study done?" If you are under 55 or no cause was found: "Have antiphospholipid antibodies been tested and repeated, and have the young-stroke tests — Fabry, CADASIL if the MRI fits, syphilis and HIV, a vasculitis screen — been considered?" And for any test offered: "What would the result change?"
7. Where UK and US guidance differ
The 2026 US acute guideline adds troponin to the routine first-day bloods and says lipids need not be fasting; UK practice already did both. The US secondary-prevention guideline is more explicit about HIV and syphilis testing in young stroke and about Fabry testing in cryptogenic young stroke; NCGS 2023 has dedicated CADASIL and amyloid angiopathy sections the US guideline lacks. Both recommend lipoprotein(a) once, both reject MTHFR and routine thrombophilia panels for arterial stroke, and both confine genetic testing to a clinical or family clue.