8th August 2024

Stroke

Overview of stroke

This is a common neurological disorder with an incidence of 100,000 people per year in the UK. It is an acute onset vascular event resulting in damage to neurological tissue. The aetiology may be ischaemic or haemorrhagic. Strokes may be further classified by symptoms and signs according to the Oxfordshire Community Stroke Project (Bamford) classification, by the lobes affected, or by a number of clinical syndromes.

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)

Haemorrhagic stroke

Aetiology and pathophysiology of haemorrhagic stroke

Approximately 20% of strokes are haemorrhagic.

The biggest risk factors are increasing age, hypertension, and use of antiplatelets or anticoagulants. Other risk factors include male sex, heavy alcohol use, stimulant drug use (cocaine), vascular malformations and cerebral malignancy, cerebral amyloid angiopathy (CAA), bleeding disorders, cerebral vasculitis and increased aneurysm risk (e.g. in connective tissue diseases or autosomal dominant polycystic kidney disease).

Haemorrhagic stroke may occur due to:

• Spontaneous intracerebral haemorrhage, risk factors for which are listed above, but most common aetiologies are hypertensive (resulting small vessel disease affecting deep perforating vessels leads to haemorrhage within the deep structures of the brain, such as the basal ganglia) and CAA (deposition of amyloid beta-peptide deposits in blood vessels results in lobar haemorrhage affecting cortical vessels. CT may demonstrate typical ‘finger-like’ projections and subarachnoid extension).
• Subarachnoid haemorrhage (SAH): mostly due to aneurysm rupture.

Pathology due to traumatic haemorrhage (e.g. subdural or extradural haematoma) is not usually considered a stroke.

Presentation and management of haemorrhagic stroke

The presentation is similar to ischaemic stroke. Clues that a stroke may be haemorrhagic include meningism, severe headache, reduced or progressive loss of consciousness and seizures.

Initial assessment is the same as for ischaemic stroke, including the importance of swift diagnosis and management. Specific considerations for haemorrhagic stroke include:

• Assessment: haemorrhage will usually be seen on CT
• Initial treatment:
  • Rapid blood pressure control using IV labetalol, target 140 mmHg systolic
  • Rapid reversal of anticoagulation; not for aspirin or other antiplatelets
  • Discuss with neurosurgery
• SAH: additionally treated with nimodipine PO/NG (nasogastric) to reduce vasospasm; ultimately requires neurosurgical management with endovascular coiling, if there is an appropriate aneurysm target, to prevent re-bleeding
• Identifying the cause:
  • MRI may demonstrate an arteriovenous malformation (AVM); microbleeds suggest CAA
  • SAH: cerebral angiography (CTA, MRA [MR angiography] or digital subtraction angiography) to identify aneurysms
• Secondary prevention is with adequate control of hypertension and other risk factors. Statins are contra-indicated post haemorrhagic stroke

Image Source: Wikimedia Commons (2008). Intracerebral, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Intracerebral.jpg (Accessed: 16 January 2024)

Image Source: Wikimedia Commons (2006). Subarachnoid haemorrhage, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Subarachnoid_haemorrhage.jpg (Accessed: 16 January 2024)

Image Source: Wikimedia Commons (2016). Trauma subdural arrows, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Trauma_subdural_arrows.jpg (Accessed: 16 January 2024)

Image Source: Wikimedia Commons (2011). 13049 2011 Article 474 Fig2 HTML, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:13049_2011_Article_474_Fig2_HTML.webp (Accessed: 16 January 2024)

Stroke mimics

Common stroke mimics to consider in the differential include TIA, hypoglycaemia, migraine, seizure and postictal state, conversion disorders, malignancy, sepsis, vasculitis, Bell’s palsy or decompensation of prior stroke and mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS).

Vertigo

It may be difficult to discern a posterior circulation stroke from its differentials. For persistent vertigo in the absence of other neurology, the HINTS (head impulse, nystagmus, test of skew) examination can be used to differentiate central from peripheral causes. However, often an MRI scan is required. Key differentials and features include:

References

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• Caplan LR. Posterior circulation cerebrovascular syndromes. In: Biller J, Dashe JF, editors. UpToDate. [Internet]. Waltham (MA): UpToDate Inc; 2021. [June 8 2021; cited January 21 2022]. Available from: https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes
• Charnnarong Suwanwela N. Moyamoya disease: Etiology, clinical features and diagnosis. In: Biller J, Nordli DR, Tung GA, editors. UpToDate. [Internet]. Waltham (MA): UpToDate Inc; 2020. [Oct 21 2020; cited March 7 2022]. Available from: https://www.uptodate.com/contents/moyamoya-disease-etiology-clinical-features-and-diagnosis#H21
• Furman JM. Causes of Vertigo. In: Aminoff MJ, Deschler DG, Wilterdink JL, editors. UpToDate. [Internet]. Waltham (MA): UpToDate Inc; 2021. [March 23 2021; cited January 21 2022]. Available from: https://www.uptodate.com/contents/causes-of-vertigo
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• National Institute for Health and Care Excellence. Stroke and transient ischaemic attack in over 16s: diagnosis and initial management. London: NICE, 2019 [May 1 2019; cited January 21 2022]. Available from: https://www.nice.org.uk/guidance/ng128
• O’Ferrall E. Mitochondrial myopathies: Clinical features and diagnosis. UpToDate [Internet]. Shefner JM, Hahn S, editors. UpToDate. 2021 [cited 2022 Feb 5]. Available from: https://www.uptodate.com/contents/mitochondrial-myopathies-clinical-features-and-diagnosis
• Oliveira-Filho J, Mullen MT. Initial assessment and management of acute stroke. In: Kasner SE, Edlow JA, Dashe JF, editors. UpToDate. [Internet]. Waltham (MA): UpToDate Inc; 2021. [March 5 2021; cited January 21 2022]. Available from: https://www.uptodate.com/contents/initial-assessment-and-management-of-acute-stroke