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Cerebrovascular events


Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Stroke article more useful, or one of our other health articles.

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What is a cerebrovascular event?

A cerebrovascular event (stroke) is a clinical syndrome caused by disruption of blood supply to the brain, characterised by rapidly developing signs of focal or global disturbance of cerebral functions, lasting for more than 24 hours or leading to death. A transient ischaemic attack (TIA) refers to a similar presentation that resolves within 24 hours.

A stroke results either from ischaemic infarction of part of the brain or from intracerebral haemorrhage. Ischaemic infarction may be caused by atheroma or thromboembolism and, more rarely, by trauma, infection or tumours.

  • Cerebral infarction accounts for about 85% of strokes.1

  • Posterior circulation stroke accounts for 20-25% of ischaemic strokes.2

  • Primary haemorrhage accounts for about 10%.3

  • Subarachnoid haemorrhage accounts for approximately 5%.

  • The remainder are of uncertain type.

The two main types of stroke are not reliably distinguishable clinically but pointers include:

  • Haemorrhagic stroke: meningism, severe headache and coma within hours.

  • Ischaemic stroke: carotid bruit, atrial fibrillation, past TIA.

Cerebrovascular event causes (aetiology)

Young patient

  • Vasculitis.

  • Thrombophilia.

  • Subarachnoid haemorrhage.

  • Venous sinus thrombosis.

  • Carotid artery dissection - eg, via near-strangling or fibromuscular dysplasia.

Older patient

  • Thrombosis in situ.

  • Athero-thromboembolism - eg, from carotid arteries.

  • Heart emboli (particularly associated with atrial fibrillation, infective endocarditis or myocardial infarction).

  • Central nervous system (CNS) bleed (associated with hypertension, head injury, aneurysm rupture).

  • Sudden blood pressure drop by more than 40 mm Hg.

  • Vasculitis - eg, giant cell arteritis.

  • Venous sinus thrombosis.

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Stroke is a major health problem in the UK:

  • Stroke is the fourth most common single cause of death in the UK and the third most common in Scotland.4

  • In the UK, over 100,000 people have a first or recurrent stroke each year.

  • A conservative estimate for the incidence of first-ever TIA in the UK is 50 per 100,000 population per year.1

  • More than 900,000 people in England are living with the effects of stroke and about half of these people are dependent on other people for help with everyday activities.

  • Over 75% of stroke survivors have residual arm weakness; almost 75% leg weakness; around 1 in 3 some level of aphasia and 1 in 5 residual visual symptoms.4

  • Strokes can occur at any age but most strokes occur in people older than 65 years. Around 1 in 4 strokes affect people of working age.4

Risk factors

  • Hypertension.

  • Smoking.

  • Diabetes mellitus.

  • Heart disease (valvular, ischaemic, atrial fibrillation).

  • Peripheral arterial disease.

  • Post-TIA (TIAs are associated with a high early risk of stroke).5

  • Polycythaemia vera.

  • Carotid artery occlusion; carotid bruit.

  • Combined oral contraceptive pill.

  • Hyperlipidaemia.

  • Excess alcohol.

  • Clotting disorders.

Cerebrovascular event symptoms

  • Either sudden onset or a step-wise progression of stroke symptoms and signs over hours (or even days) is typical.

  • In people with sudden onset of neurological symptoms, a validated tool, such as FAST (Face, Arm, Speech, Time to call 999/112/911), should be used outside hospital to screen for a diagnosis of stroke or TIA.6

  • Focal signs relate to distribution of the affected artery but collateral supplies may cause variation in the presentation.

  • Cerebral hemisphere infarcts may cause:

    • Contralateral hemiplegia which is initially flaccid (floppy limb, falls like a dead weight when lifted) and then becomes spastic.

    • Contralateral sensory loss.

    • Homonymous hemianopia.

    • Dysphasia.

  • Posterior circulation ischaemia:2

    • Motor deficits (weakness, clumsiness, or paralysis of any combination of arms and legs, up to quadriplegia, sometimes changing from one side to another in different attacks).

    • 'Crossed' syndromes: ipsilateral cranial nerve dysfunction and contralateral long motor or sensory tract dysfunction.

    • Sensory deficits: numbness, including loss of sensation or paraesthesia in any combination of extremities, sometimes including all four limbs or both sides of the face or mouth.

    • Homonymous hemianopia.

    • Ataxia, imbalance, unsteadiness, or disequilibrium.

    • Vertigo, with or without nausea and vomiting.

    • Diplopia (ophthalmoplegia).

    • Dysphagia or dysarthria.

    • Isolated reduced level of consciousness can result from bilateral thalamic or brain stem ischaemia.

    • Complete infarction affecting the pons causes 'locked-in syndrome' with quadriparesis, loss of speech, but preserved awareness and cognition, and sometimes preserved eye movements.

  • Lacunar infarcts (25%):

    • Small infarcts around the basal ganglia, internal capsule, thalamus and pons.

    • May cause pure motor, pure sensory, or mixed motor and sensory signs, or ataxia.

    • Intact cognition/consciousness.

Dysphagia affects a large proportion of stroke patients, with prevalence ranging from 50-80%.7

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Differential diagnosis


  • FBC - thrombocytopenia, polycythaemia.

  • Test for sickle cell disease.

  • Erythrocyte sedimentation rate (ESR) - giant cell arteritis (consider temporal lobe artery biopsy, start steroids).

  • Hypoglycaemia, hyperglycaemia and hyperlipidaemia.

  • Syphilis - active, untreated.

  • Hypertension:

    • Hypertensive retinopathy.

    • Large heart on CXR.

    • Ventricular hypertrophy on ECG.

  • Emboli from the left atrium may have caused the stroke. Look for a large left atrium on CXR and consider echocardiography.

  • Post-myocardial infarction - mural thrombus is best shown by echocardiography.

  • Brain imaging should be undertaken as soon as possible (and within 24 hours or symptom onset) in all patients. Brain imaging with non-enhanced CT should be undertaken immediately if the patient:6

    • Has indications for thrombolysis or early anticoagulant treatment.

    • Is currently taking anticoagulant treatment.

    • Has a known bleeding tendency.

    • Has a depressed level of consciousness (Glasgow Coma Score below 13).

    • Has unexplained progressive or fluctuating symptoms.

    • Has papilloedema, neck stiffness or fever.

    • Has severe headache at onset of stroke symptoms.

  • Imaging with CT contrast angiography should also be performed if thrombectomy might be indicated.6

  • Scanning should be performed as soon as possible and within 24 hours of symptom onset in everyone with suspected acute stroke without indications for immediate brain imaging.

  • Infective endocarditis: 20% of those with endocarditis present with CNS signs due to septic emboli from valves.

  • Carotid duplex ultrasound: in stroke or TIA in carotid territory.

Cerebrovascular event treatment and management

Acute stroke management

  • Patients should be admitted to hospital (ideally a specialist acute stroke unit for initial care and treatment, unless the diagnosis will make no difference to management - eg, where the optimal management is palliative care).8

  • Maintenance or restoration of homeostasis:6

    • Oxygen therapy; give supplemental oxygen only if oxygen saturation drops below 95%.

    • Blood sugar control; maintain blood glucose concentration between 4 and 11 mmol/L. Provide optimal insulin therapy with intravenous insulin and glucose, for people with diabetes.

    • Blood pressure control for people with acute ischaemic stroke:

      • Blood pressure reduction to 185/110 mm Hg or lower should be considered in people who are candidates for intravenous thrombolysis.6

      • There is currently insufficient evidence to reliably evaluate the effect that altering blood pressure has on the outcome after acute stroke.9

      • For people with acute intracerebral haemorrhage who present within six hours and have a systolic blood pressure of 150-220 mm Hg (unless there is a structural cause for the haemorrhage or they have a poor expected prognosis or Glasgow Coma Scale score of below 6), offer rapid blood pressure lowering, aiming for systolic pressure of 130-140 mm Hg maintained for at least seven days.6

      • Give antihypertensive treatment only if there is a hypertensive emergency with one or more of the following:

        • Hypertensive encephalopathy.

        • Hypertensive nephropathy.

        • Hypertensive cardiac failure/myocardial infarction.

        • Aortic dissection.

        • Pre-eclampsia/eclampsia.

    • Blood pressure control for people with acute intracerebral haemorrhage:6

      • Do not offer rapid blood pressure lowering if people have had acute intracerebral haemorrhage and:

        • Have an underlying structural cause (eg tumour, arteriovenous malformation or aneurysm).

        • Have a score on the Glasgow Coma Scale of below 6.

        • Are going to have early neurosurgery to evacuate the haematoma.

        • Have a massive haematoma with a poor expected prognosis.

      • Consider rapid blood-pressure lowering for people with acute intracerebral haemorrhage with none of the exclusions above who:

        • Present within six hours of symptom onset; and

        • Have a systolic blood pressure of 150-220 mm Hg.

      • For other patients without the exclusions above, consider rapid blood-pressure lowering (on a case-by-case basis, taking into account the risk of harm) for people who:

        • Present more than six hours from symptom onset; or

        • Have a systolic blood pressure above 220 mm Hg.

      • When lowering blood pressure rapidly in these patients, ensure that the magnitude drop does not exceed 60 mm Hg within one hour of commencing treatment, while aiming for a systolic blood pressure of ≤140 mm Hg.

      • Seek advice from a paediatric specialist when considering blood-pressure lowering in 16- to 17-year-olds with acute intracerebral haemorrhage without any of the exclusions above.

  • People with acute stroke should have their swallowing screened before being given any oral food, fluid or medication. Also screen for malnutrition.1

  • Antiplatelet therapy:

    • Aspirin 300 mg daily, unless contra-indicated, should be offered to people who have had a suspected TIA, and started immediately.6

    • Aspirin (300 mg) should be given as soon as possible after the onset of stroke symptoms once a diagnosis of primary haemorrhage has been excluded.10

  • For long-term vascular prevention in people with ischaemic stroke or TIA without paroxysmal or permanent atrial fibrillation:1

    • Clopidogrel 75 mg daily should be the standard antithrombotic treatment.

    • Aspirin 75 mg daily with modified-release dipyridamole 200 mg twice daily should be used for those who are unable to tolerate clopidogrel:

      • Aspirin 75 mg daily should be used if both clopidogrel and modified-release dipyridamole are contra-indicated or not tolerated.

      • Modified-release dipyridamole 200 mg twice daily should be used if both clopidogrel and aspirin are contra-indicated or not tolerated.

  • Thrombolytic treatment: see the separate Thrombolytic Treatment of Acute Ischaemic Stroke article. Unless there are contra-indications, thrombolytic treatment appears to be effective in improving prognosis after an acute stroke.11 Treatment with alteplase should only be given provided that:

    • It is administered within four and a half hours (preferably within three hours) of onset of stroke symptoms.1

    • Haemorrhage has been definitively excluded.

    • There is immediate access to imaging and re-imaging, including staff trained to interpret the results.6

  • Anticoagulants should not be started until brain imaging has excluded haemorrhage. In patients with acute ischaemic stroke, immediate anticoagulant therapy is not associated with any overall short-term or long-term benefit. Treatment with anticoagulants reduces recurrent stroke, deep vein thrombosis and pulmonary embolism but increases bleeding risk. Therefore, anticoagulants should not be used routinely for patients with acute ischaemic stroke.12

  • Drugs depressing the function of the CNS (eg, anxiolytics and tranquilisers) and new prescriptions for sedatives should be avoided.

  • Do not start statin treatment immediately after an acute stroke but continue statin treatment for people with acute stroke who are already taking statins.6

  • Encourage the person to sit out of bed and mobilise as soon as their clinical condition permits, as part of an active management programme.6

  • High-intensity mobilisation should not be offered in the first 24 hours to people who need help to sit out of bed, stand or walk.6

  • Patients with TIA, or patients with a stroke who have made a good recovery when seen, should be assessed and investigated in a specialist service (eg, a neurovascular clinic) as soon as possible and within seven days of the incident.

Subarachnoid haemorrhage

Subarachnoid haemorrhage should be considered in any patient presenting with sudden-onset, severe and unusual headache with or without any associated alteration in consciousness. See the separate Subarachnoid Haemorrhage article.

Surgical management

  • Thrombectomy should be offered as soon as possible (and within six hours of symptom onset to patients with confirmed ischaemic stroke with occlusion of the proximal anterior circulation.6

  • If there is potential to salvage brain tissue (as shown by imaging) the patients above should also be considered for thrombectomy between 6 and 24 hours after symptom onset, if they were known to be well beforehand.6

  • Thrombectomy should also be considered as soon as possible (and up to 24 hours after symptom onset) for patients with confirmed ischaemic stroke occluding the proximal posterior circulation if there is potential to salvage brain tissue.6

  • Thrombectomy should usually only be considered in patients with:

    • A pre-stroke functional status of less than 3 on the modified Rankin scale; and

    • A score of more than 5 on the National Institutes of Health Stroke Scale NIHSS).6

  • Surgical intervention should be considered in cases of supratentorial haemorrhage with mass effect or posterior fossa/cerebellar haematoma.

  • Neurosurgical opinion should be sought for cases of secondary hydrocephalus.

  • Carotid endarterectomy: see the separate Carotid Artery Stenosis and Stroke Prevention articles.

  • There is currently insufficient evidence to support intracranial stenting, unless part of research protocol.13

  • Consider referring for surgical decompressive hemicraniectomy (performed within 48 hours of symptom onset) if middle cerebral artery (MCA) infarction is present and all the following are met:

    • Clinical deficits suggestive of infarction in the territory of the MCA.

    • Score of above 15 on the NIHSS.

    • Decrease in the level of consciousness.

    • Signs on CT scan of an infarct of at least 50% of MCA territory with infarct volume greater than 145 cm3 as shown on diffusion-weighted MRI.6

Secondary prevention of stroke and TIAs

See the separate Stroke Prevention article.

Long-term management

See the separate Cerebrovascular Event Rehabilitation article.


  • Neurological problems: balance, movement, tone and sensation.

  • Pain: neuropathic and/or musculoskeletal.

  • Depression, anxiety, emotionalism, disturbed social interaction, disinhibition, aggression.

  • Cognitive impairments: attention and concentration, memory, disturbances of spatial awareness, disturbance of perception (eg, visual agnosia), apraxia and disturbances of executive functioning (planning, organising, initiating and monitoring behaviour).

  • Speech and communication difficulties: dysphasia, dysarthria, and apraxia of speech.

  • Visual impairments and hemianopia.

  • Bladder and bowel problems: urinary incontinence, faecal incontinence, constipation.

  • Swallowing problems, poor oral health, malnutrition, dehydration.

  • Sexual dysfunction .

  • Difficulties with activities of daily living: personal, social and vocational.

  • Other complications include thromboembolism, pneumonia and bedsores

Dysphagia, in addition to poor oral health and reduced ability to self-feed, will affect nutrition in people with stroke. In addition, people with dysphagia after an acute stroke are at higher risk of aspiration pneumonia. To avoid aspiration pneumonia, give food, fluids and medication to people with dysphagia in a form that can be swallowed without aspiration, after specialist assessment of swallowing.6

NB: morbidity within carers is high - in particular stress, which is only partly relieved by respite admissions.


  • 85% of stroke patients in England, Wales and Northern Ireland survive to hospital discharge.

  • 2 in 3 stroke survivors either have supported community discharge or return home on hospital discharge.

  • Almost 2 in 3 stroke survivors leave hospital with a disability.

  • 4 in 10 stroke survivors require help with activities of daily living on discharge.

  • Approximately 1 in 4 stroke survivors will have another stroke within five years.

  • The proportion of the UK population who are stroke survivors ranges from 1.7% in England to 2.2% in Scotland.

  • Approximately half of stroke survivors have residual:

    • Swallowing problems.

    • Bladder or bowel dysfunction.

    • Fatigue.

  • 1 in 3 stroke survivors experience depression and 1 in 5 experience anxiety symptoms.

  • Stroke suvivors of working age are 2-3 times more likely to be unemployed eight years after their stroke than non-affected members of the population.

  • The inpatient death rate for people admitted with a stroke is about 24%. The risk of stroke recurring within 30 days of an ischaemic stroke depends on the cause of the stroke:

    • Stroke caused by large-vessel cervical or intracranial atherosclerosis with stenosis - risk about 20%.

    • Cardioembolic stroke - risk about 5%.

    • Lacunar stroke - risk about 1%.

  • Basilar occlusion is associated with high mortality or severe disability, especially if blood flow is not restored in the vessel.2

Cerebrovascular event prevention

See the separate Stroke Prevention and Primary Prevention of Cardiovascular Disease articles.

ABCD prognostic score for people with a TIA1

Total scores range from 0 (low risk) to 7 (high risk):

  • Age (1 point where aged 60 years or over).

  • Blood pressure (1 point for blood pressure of 140/90 mm Hg, or higher).

  • Clinical features (2 points for unilateral weakness; 1 point for speech disturbance without weakness).

  • Duration of symptoms (2 points for 60 minutes or longer; 1 point for 10-59 minutes).

1 point is added for the presence of diabetes.

However NICE recommends not using scoring systems, such as ABCD2, to assess risk of subsequent stroke or to inform urgency of referral for people who have had a suspected or confirmed TIA.6

General Medical Services Contract Quality Framework audit criteria

Quality and Outcomes Framework guidance: stroke and TIA (2019/20).14

  • Establish and maintain a register of patients with stroke or TIA. 2 points.

  • The percentage of patients with a stroke shown to be non-haemorrhagic, or a history of TIA, who have a record in the preceding 12 months that an antiplatelet agent, or an anticoagulant is being taken. Achievement threshold 57-97%. 4 points.

  • The percentage of patients with stroke or TIA who have had influenza immunisation in the preceding 1 August to 31 March. Achievement threshold 55-95%. 2 points.

  • The percentage of patients aged 79 years or under with a history of stroke or TIA in whom the least blood pressure reading (measured in the preceding 12 months) is 140/90 mm Hg or less. Achievement threshold 40-73%. 3 points.

  • The percentage of patients aged 80 years and over with a history of stroke or TIA in whom the last blood pressure reading (measured in the preceding 12 months) is 150/90 mm Hg or less. Achievement threshold 46-86%. 2 points.

Further reading and references

  1. Stroke Guidelines; Royal College of Physicians (2016)
  2. Merwick A, Werring D; Posterior circulation ischaemic stroke. BMJ. 2014 May 19;348:g3175. doi: 10.1136/bmj.g3175.
  3. Andersen KK, Olsen TS, Dehlendorff C, et al; Hemorrhagic and ischemic strokes compared: stroke severity, mortality, and risk factors. Stroke. 2009 Jun;40(6):2068-72. doi: 10.1161/STROKEAHA.108.540112. Epub 2009 Apr 9.
  4. State of the Nation - Stroke statistics; Stroke Association 2017
  5. Ovbiagele B, Cruz-Flores S, Lynn MJ, et al; Early stroke risk after transient ischemic attack among individuals with symptomatic intracranial artery stenosis. Arch Neurol. 2008 Jun;65(6):733-7.
  6. Stroke and transient ischaemic attack in over 16s: diagnosis and initial management; NICE Guidance (May 2019 - last updated April 2022)
  7. Kim D-Y, Park H-S, Park S-W et al. The impact of dysphagia on quality of life in stroke patients. Medicine 2020: 99 (34); e21795 doi: 10.1097/MD.0000000000021795
  8. No authors listed; Organised inpatient (stroke unit) care for stroke. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD000197.
  9. Geeganage C, Bath PM; Vasoactive drugs for acute stroke. Cochrane Database Syst Rev. 2010 Jul 7;(7):CD002839.
  10. Sandercock PA, Counsell C, Gubitz GJ, et al; Antiplatelet therapy for acute ischaemic stroke. Cochrane Database Syst Rev. 2008 Jul 16;(3):CD000029.
  11. Wardlaw JM, Murray V, Berge E, et al; Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev. 2009 Oct 7;(4):CD000213.
  12. Sandercock PA, Counsell C, Kamal AK; Anticoagulants for acute ischaemic stroke. Cochrane Database Syst Rev. 2008 Oct 8;(4):CD000024.
  13. Endovascular stent insertion for intracranial atherosclerotic disease; NICE Interventional procedures guidance, July 2012
  14. 2019/20 General Medical Services (GMS) contract Quality and Outcomes Framework (QOF); NHS England/BMA, April 2019

Article history

The information on this page is written and peer reviewed by qualified clinicians.

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