8th August 2024

Ischaemic stroke

Aetiology of ischaemic stroke

Ischaemic stroke accounts for 80% of cases. Risk factors include increasing age, (family) history of stroke, smoking, hypertension, diabetes, atrial fibrillation, ischaemic heart disease, hypercholesterolaemia and sickle cell disease.

Ischaemic stroke may occur due to:

• Large vessel atherosclerosis resulting in thromboembolism
• Cardioembolism: atrial fibrillation, endocarditis, myocardial infarction, paradoxical systemic emboli
• Small vessel occlusion

Rarer aetiologies include:

• Venous infarction: this is caused by cerebral venous sinus thrombosis (CVST). Risk factors include oral contraception, dehydration, malignancy, thrombophilia and infection. It results in infarction with significant oedema and presents with headache, focal neurology and seizures. The pathology does not follow usual arterial infarct territories, and the empty delta sign on CT venogram is diagnostic. Patients are prone to haemorrhage but treatment is with anticoagulation (heparin then warfarin).
• Carotid and vertebral artery dissection: separation of the arterial walls results in haematoma formation. This may be spontaneous, related to trauma to the neck, which may be minor or not remembered (can include neck manipulation, sports and childbirth) or fibromuscular dysplasia. Resultant ischaemia is usually due to thromboembolism.
• Border zone infarct: a sudden drop in systemic blood pressure and subsequent intracerebral perfusion, for example with sepsis, may result in a border zone infarct in areas at the periphery of vascular territories.
• Inherited disorders including cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), an inherited disorder of the NOTCH3 gene resulting in migraine with aura, ischaemic events and cognitive impairment.
• Dolichoectasia (elongation and tortuosity) of the vertebrobasilar arteries, leading to thrombus formation.
• Moyamoya disease: a disease characterised by large vessel intracranial stenosis and subsequent collateral formation resulting in a classical ‘puff of smoke’ appearance on angiography. Unknown cause, highest prevalence in East Asian countries.
• In the context of systemic disease: vasculitis, thrombophilia.

Presentation of ischaemic stroke

The exact presentation varies depending on the vascular territory affected but, importantly, strokes cause sudden onset (within seconds) of negative symptoms. These include sensory deficit, motor deficit, speech impairment and visual impairment.

General clinical features according to the territory affected, as well as key stroke syndromes, are outlined below.

Anterior circulation (supplied by the internal carotid arteries, ICA):

Posterior circulation (vertebrobasilar circulation):

Assessment of ischaemic stroke

Timely diagnosis and management of stroke is crucial as the longer from the acute event, the more brain tissue is irreversibly damaged, and earlier initiation of treatment is associated with better outcomes.

• Recognition: using a validated score such as ROSIER (Recognition of Stroke in the Emergency Room) or FAST (Face Arm Speech Test) in the community.
• Assessment: a focused history from the patient or witness and an examination using the National Institutes of Health Stroke Scale (NIHSS) is performed to give an indication of stroke severity.
• Bedside tests: routine bloods including clotting, blood glucose to exclude mimic, ECG for arrhythmias.
• Imaging: immediate non-contrast CT head to exclude haemorrhage, consider CT angiography (CTA) if a large-vessel occlusion is suspected or the patient is a candidate for thrombectomy (see below).

Management of ischaemic stroke

Initial treatment should be supportive: monitor blood pressure, saturations, glucose and GCS, treat seizures if occurring, make nil by mouth until swallow assessment is performed. The patient should be admitted to a hyperacute stroke unit (HASU).

Specific management depends on time of onset:

Secondary prevention:

• Antiplatelet or anticoagulant: clopidogrel monotherapy lifelong or consider DOAC after 14 days if indicated (e.g. in AF)
• Carotid endarterectomy within 2 weeks if there is significant symptomatic stenosis, defined as >50% symptomatic stenosis using the NASCET criteria or > 70% stenosis using the ECST criteria. If there is contralateral stenosis, elective surgery may be offered after two to four weeks
• High-intensity statin therapy
• Control of vascular risk factors, including diabetes, hypertension and smoking

Further investigations and identifying an underlying cause

• MRI scan: diffusion-weighted imaging (DWI) is sensitive for an acute infarct
• Cardiac monitoring: to identify arrhythmias; consider Holter (ambulatory) monitor if suspicion of an embolic source (e.g. bilateral infarcts) but no arrhythmia has been captured during admission
• Echo: to identify vegetations, which can be a source of emboli; consider bubble echo to identify patent foramen ovale as source of paradoxical embolus
• Carotid Doppler: for large vessel atherosclerosis or dissection
• Bloods: in a younger patient, consider additional bloods such as a vasculitis screen and HIV and syphilis serology. Test for conditions such as polycythaemia, thrombophilia or sickle cell disease if appropriate

Complications of ischaemic stroke

• Malignant transformation: if a patient suffers a large MCA or cerebellar stroke the resulting oedema may cause raised intracranial pressure and herniation, which requires immediate neurosurgical discussion.
• Haemorrhagic transformation: large infarcts have a tendency to bleed, particularly if given thrombolysis. Monitor for neurological deterioration and immediately repeat a CT brain if this occurs.

Image Source: Wikimedia Commons (2016). DWE MRI of cerebral infarctio, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:DWE_MRI_of_cerebral_infarction.png (Accessed: 16 January 2024)