A cerebrovascular event (stroke) is a clinical syndrome of presumed vascular origin, typified by rapidly developing signs of focal or global disturbance of cerebral functions. It lasts more than 24 hours or leads to death.

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 70% of strokes.
• Primary haemorrhage is about 15%.
• Subarachnoid haemorrhage is approximately 5%.
• The remainder is of uncertain type.¹

Aetiology

Young patient

• Vasculitis.
• Thrombophilia.
• Subarachnoid haemorrhage.
• Venous-sinus thrombosis.
• Carotid artery dissection, e.g. via near-strangling or fibromuscular dysplasia.

Older patient

• Thrombosis in situ.
• Athero-thromboembolism, e.g. 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, e.g. giant cell arteritis.
• Venous-sinus thrombosis.

Epidemiology

Stroke is a major health problem in the UK:

• An estimated 150,000 people have a stroke in the UK each year.
• There are over 67,000 deaths due to stroke each year in the UK.
• Each year in England, approximately 110,000 people have a first or recurrent stroke and a further 20,000 people have a transient ischaemic attack (TIA).²

Risk factors

• Hypertension.
• Smoking.
• Diabetes mellitus.
• Heart disease (valvular, ischaemic, atrial fibrillation).
• Peripheral vascular disease.
• Past TIA (approximately 15% of ischaemic strokes are preceded by a TIA with the greatest risk within the first 72 hours after the TIA).³
• Polycythaemia vera.
• Carotid artery occlusion; carotid bruit.
• Combined oral contraceptive pill.
• Hyperlipidaemia.
• Excess alcohol.
• Clotting disorders.

Presentation

• Either sudden onset or a step-wise progression of 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 Test), should be used outside hospital to screen for a diagnosis of stroke or TIA.²
• Focal signs relate to distribution of the affected artery, but collateral supplies may cause variation in the presentation.
• Cerebral hemisphere infarcts (50%) 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.
• Brainstem infarction (25%):
  • A wide range of effects which include quadriplegia, disturbances of gaze and vision, locked-in syndrome (aware but unable to respond).
  • Lateral medullary syndrome from vertebrobasilar occlusion.
• Lacunar infarcts (25%):
  • Small infarcts around the basal ganglia, internal capsule, thalamus and pons.
  • May cause pure motor, pure sensory, mixed motor and sensory signs, or ataxia.
  • Intact cognition/consciousness.

Differential diagnosis

• The two 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.
• CNS tumour.
• Subdural bleed.
• Todd's palsy.
• Consider a drug overdose if the patient is comatose.

Investigations

• 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.
  NB: raised blood pressure may be an acute result of stroke, and therefore should not be treated unless sustained. Treatment of raised blood pressure soon after a stroke may lead to a worse prognosis.⁴
• 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. In stroke due to atrial fibrillation or mural thrombus, a CT scan should be performed to exclude a haemorrhagic stroke, and then aspirin started.⁵
• Brain imaging should be undertaken as soon as possible in all patients, at least within 24 hours of onset unless there are good clinical reasons for not doing so. Brain imaging should be undertaken immediately if the patient:¹
  • Is currently taking anticoagulant treatment.
  • Has a depressed level of consciousness (Glasgow Coma Score below 13).
  • Has papilloedema, neck stiffness or fever.
  • Has indications for thrombolysis or early anticoagulation.
  • Has a known bleeding tendency.
  • Has unexplained progressive or fluctuating symptoms.
  • Has severe headache at onset.
• CT scanning:
  • A CT scan provides evidence of haemorrhage within the first 48 hours in up to 98% of patients with subarachnoid haemorrhage.
  • CT scan is considered superior to MRI in this context.⁶
• 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.

Management

Acute stroke management

• Patients should be admitted to hospital (ideally a stroke unit for initial care and treatment, unless the diagnosis will make no difference to management, e.g. where the optimal management is palliative care).⁷
• Maintenance or restoration of homeostasis:²
  • 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; 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.
    • Intracerebral haemorrhage with systolic blood pressure >200 mm Hg.
  • Consider blood pressure reduction to 185/110 mm Hg or lower in people who are candidates for thrombolysis.
• People with acute stroke should have their swallowing screened before being given any oral food, fluid or medication. Also screen for malnutrition.¹
• 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.⁸ Antiplatelet therapy should then be continued indefinitely. Aspirin should be delayed for 24 hours following thrombolysis.
• Anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke.⁹
• Unless there are contra-indications, thrombolytic treatment appears to be effective in improving prognosis after an acute stroke.¹⁰ Treatment with alteplase should only be given provided that:
  • It is administered within three hours of onset of stroke symptoms (unless as part of a clinical trial).²
  • Haemorrhage has been definitively excluded.
• Drugs depressing the function of the CNS (e.g. 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.²
• Encourage the person to sit up and mobilise as soon as their clinical condition permits.²
• 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 (e.g. a neurovascular clinic) as soon as possible within seven days of the incident.

Secondary prevention of stroke and TIAs

See Stroke Prevention article.

Long-term management

Please see separate article Cerebrovascular Event Rehabilitation.

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.

• If subarachnoid haemorrhage is suspected:
  • CT brain scan: immediately if the patient has impaired consciousness and within 12 hours in all patients. If the CT scan is negative or equivocal, lumbar puncture should be undertaken 12 or more hours after onset. Spectrophotometry should be used to permit detection of small amounts of xanthochromia.
  • An MRI brain scan should not be used to diagnose subarachnoid haemorrhage.
• Once the diagnosis is confirmed:
  • Oral nimodipine 60 mg four-hourly is given, unless there are specific contra-indications.
  • Anti-fibrinolytic agents and steroids should not be given.
  • All patients should be discussed with a neurosurgeon immediately.
  • Imaging of cerebral vessels should be undertaken at the neurosciences centre.
  • A ruptured aneurysm should be treated by endovascular or surgical obliteration as determined by the neurovascular team.
  • All patients should be monitored for the development of treatable complications, especially hydrocephalus, cerebral ischaemia, electrolyte imbalance and hypotension.

Surgical

• 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:¹¹
  • Any patient with a carotid artery territory stroke but without severe disability should be considered for carotid endarterectomy.
  • Carotid duplex ultrasound should be performed on all patients being considered for carotid endarterectomy and confirmed with magnetic resonance angiography or with a second ultrasound.
  • Carotid endarterectomy should be considered where carotid stenosis is measured at greater than 70%, as measured using the European Carotid Surgery Trialists' methods, and 50%, as measured using the North American Symptomatic Carotid Endarterectomy Trial Collaborators' methods.
  • Carotid endarterectomy should be performed within 2 weeks of the cerebrovascular event.²
  • Carotid angioplasty or stenting is an alternative to surgery but should only be carried out in specialist centres.
• There is currently insufficient evidence to support intracranial stenting, unless part of research protocol.¹²
• Consider referring for surgical decompressive hemicraniectomy if middle cerebral artery (MCA) infarction is present and all the following are met (refer within 24 hours of symptom onset and perform surgery within 48 hours of symptom onset):
  • Aged 60 years or under.
  • Clinical deficits suggestive of infarction in the territory of the MCA.
  • Decrease in the level of consciousness.
  • Signs on CT scan of an infarct of at least 50% of MCA territory or infarct volume greater than 145 cm³ as shown on diffusion-weighted MRI.

Complications

• Patients who have suffered a stroke remain at an increased risk of a further stroke (between 30% and 43% risk within five years).¹ The risk of a further stroke is highest early after the stroke or TIA.¹¹
• Patients with TIA and stroke also have an increased risk of myocardial infarction and other vascular events.
• By 6 months, over half of stroke survivors will need some help with activities of daily living. 15% will have communication impairments and 53% motor weakness, and many will have problems with mood or cognition.

Other complications for the patient include thromboembolism, pneumonia, depression, contractures, bladder and bowel problems (e.g. incontinence, constipation) and bed sores.

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

Prognosis

• Most people survive a first stroke, but often have significant morbidity.
• Mortality is 20% at 1 month and then 5-10% per year thereafter.
• Drowsiness suggests a poorer prognosis.

Prevention

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

General Medical Services Contract Quality Framework audit criteria

Quality and outcomes framework guidance: stroke and TIA (April 2009):¹³

• STROKE 1: the practice can produce a register of patients with stroke or TIA: 2 points.
• STROKE 13: the percentage of new patients with a stroke who have been referred for further investigation: 2 points; payment stages 40-80%.
• STROKE 5: the percentage of patients with TIA or stroke who have a record of blood pressure in the notes in the preceding 15 months: 2 points; payment stages 40-90%.
• STROKE 6: the percentage of patients with a history of TIA or stroke in whom the last blood pressure reading (measured in the previous 15 months) is 150/90 mm Hg or less: 5 points; payment stages 40-70%.
• STROKE 7: the percentage of patients with TIA or stroke who have a record of total cholesterol in the last 15 months: 2 points; payment stages 40-90%.
• STROKE 8: the percentage of patients with TIA or stroke whose last measured total cholesterol (measured in the previous 15 months) is 5 mmol/L or less: 5 points; payment stages 40-60%.
• STROKE 12: the percentage of patients with a stroke shown to be non-haemorrhagic, or a history of TIA, who have a record that an antiplatelet agent (aspirin, clopidogrel, dipyridamole or a combination), or an anti-coagulant is being taken (unless a contra-indication or side-effects are recorded): 4 points; payment stages 40-90%.
• STROKE 10: the percentage of patients with TIA or stroke who have had influenza immunisation in the preceding 1 September to 31 March: 2 points; payment stages 40-85%.

Document references

1. National clinical guideline for stroke (third edition), Royal College of Physicians (July 2008); Prepared by the Intercollegiate Stroke Working Party, incorporating the recommendations from NICE stroke guideline
2. Stroke: The diagnosis and acute management of stroke and transient ischaemic attacks, NICE Clinical Guideline (July 2008)
3. Lovett JK et al; Very Early Risk of Stroke After a First Transient Ischemic Attack; Stroke. 2003;34:e138 - Research Report
4. Ahmed N, Wahlgren NG; Effects of blood pressure lowering in the acute phase of total anterior circulation infarcts and other stroke subtypes. Cerebrovasc Dis. 2003;15(4):235-43. [abstract]
5. Wardlaw JM et al; What is the best imaging strategy for acute stroke? Health Technology Assessment 2004; Vol 8: number 1
6. Radiology guidelines and best practice statements (various), Royal College of Radiologists (various dates)
7. No authors listed; Organised inpatient (stroke unit) care for stroke. Stroke Unit Trialists' Collaboration. Cochrane Database Syst Rev. 2000;(2):CD000197. [abstract]
8. Sandercock PA, Counsell C, Gubitz GJ, et al; Antiplatelet therapy for acute ischaemic stroke. Cochrane Database Syst Rev. 2008 Jul 16;(3):CD000029. [abstract]
9. Gubitz G, Sandercock P, Counsell C; Cochrane Review; Anticoagulants for acute ischaemic stroke, March 2004
10. Wardlaw JM, del Zoppo G, Yamaguchi T, Berge E; Cochrane Review; Thrombolysis for acute ischaemic stroke, March 2003.
11. Cina CS, Clase CM, Haynes RB; Cochrane Review; Carotid endarterectomy for symptomatic carotid stenosis, March 1999
12. Endovascular stent insertion for intracranial atherosclerotic disease, NICE Interventional Procedure Guideline (October 2007)
13. Stroke and transient ischaemic attack, Prodigy (February 2009)

Internet and further reading

• Vascular disease - clopidogrel and dipyridamole, NICE Technology Appraisal Guideline (December 2010); Clopidogrel and modified-release dipyridamole for the prevention of occlusive vascular events
• Management of patients with stroke or TIA: assessment, investigation, immediate management and secondary prevention, Scottish Intercollegiate Guidelines Network - SIGN (December 2008)
• Management of patients with stroke: Identification and management of dysphagia, Scottish Intercollegiate Guidelines Network - SIGN (June 2010)