Chapter 130: Stroke and transient ischaemic attacks

Major: hypertension, smoking, cardiovascular disease, atrial fibrillation (especially valvular), diabetes.

Others: cardiac failure, dyslipidaemia, obesity, alcohol excess, oral contraception, migraine, stress.

Control of risk factors is the key approach to management. Control of hypertension, including systolic hypertension in the elderly, and smoking cessation are vital factors for reduction of the incidence of stroke. A meta-analysis of 14 randomised trials showed that a reduction of blood pressure of 5–6 mmHg is associated with about 40% reduction in stroke incidence.¹

Stroke

Facts¹

• Stroke is the third most common cause of death in Australia.

• About one-third of people who have a stroke will die within 1 month.

• About 50% of ischaemic strokes are preceded by TIAs.

• Symptomatic carotid artery stenosis is the major risk factor for stroke.

• Thromboembolism from vascular disease outside the brain causes 70% of strokes and 90% of TIAs.

• Such sources are atheromatous plaques within the carotid or vertebral systems or cardiac causes (e.g. postmyocardial infarction).

• Echocardiography is an important investigation with TIAs since LV dysfunction and the size of the left atrium are the strongest independent predictors of thromboembolism.

Pathophysiological groups of cerebral infarction

The three main groups are:

• single penetrator or small vessel disease (lacunar syndrome)—probably due to in situ small vessel disease

• cardio–emboli (heart to artery embolism)

• large vessel artery-to-artery embolic infarcts (see TABLE 130.1)

Differential diagnosis (‘stroke mimics’)

• Syncope

• Seizure (and subsequent Todd paresis)

• Migraine

• Cerebral tumour and other space-occupying lesions

• Hypoglycaemia

• Hyponatraemia

• Delirium

• Head injury

• MELAS syndrome

• Medically unexplained (e.g. somatisation)

Diagnostic guidelines

• Sudden stroke is typical of embolism.

• The clinical picture depends on the vessel involved.

• In young people <50 years consider PFO.

• With cerebral haemorrhage the stroke evolves steadily, often over hours: the putamen (50%) is the commonest site.

• Lacunar CVAs:

  • – small, deep infarcts

  • – pure motor hemiplegia most common effect

  • – lack of cortical signs

  • – the neurological deficit may progress over 24–36 hours

  • – outcome usually good

• Investigate all, including SAH, with CT scans or MRI (may need a lumbar puncture for SAH diagnosis). MRI is preferred if available.

• Carotid duplex Doppler ultrasound scan can accurately determine atherosclerotic narrowing of the extracranial carotid circulation.

Pitfalls

• Mistaking visual or sensory migraine equivalents in young adults for TIAs

• Mistaking a CVA for labyrinthitis (rare over 50 years)

• Failure to perform carotid duplex Doppler ultrasound or CT scan before starting aspirin for TIA or small stroke (because of missing small haemorrhage, unsuspected tumour or a subdural)

• Diagnosing small stroke as a lacuna (may be a stroke in evolution)

Management

The development of an acute stroke or TIA is a medical emergency and admission to a stroke unit (if available) as soon as possible is advised. Care in a stroke unit gives the patient the greatest chance of independent survival.³

Immediate

• Stabilise ventilation—consider intubation and oxygen.

• Exclude head trauma.

• Obtain urgent CT or MRI scan (non-contrast CT scan is emerging investigation of choice).

• Treat any seizures.

• Treat any hypoglycaemia.

General

• Investigate, including carotid duplex Doppler ultrasound (for carotid territory symptoms).

• Treat hypertension (systolic >140) vigorously—it carries a six times increased risk of stroke.

• Give IV fluid, electrolyte and nutritional support (nil orally until swallowing has been assessed).

• Good nursing care is the cornerstone of management.

• Physiotherapy and speech therapy.

• Vigorous rehabilitation.

• Clot extraction for intracerebral haemorrhage: consider urgent surgical evacuation for haematomas of the posterior fossa (cerebellum) and cerebral white matter.¹ Shunt insertion may be needed. No medical therapy is of proven value.

• SAH: requires urgent referral (vasospasm and rebleeding are the main causes of morbidity and mortality):

  • – nimodipine ± surgery

• Ischaemic stroke: give aspirin 150–300 mg (o) daily within 48 hours if CT scan/MRI has excluded cerebral haemorrhage or other blood-thinning agents are not used. Early intervention within 3–4.5 hours (ideally) of onset with tissue plasminogen activator (tPA). Recent trials indicate improved outcomes with tPA (but not with streptokinase). However, there appears to be a 5–7% risk of intracerebral haemorrhage¹ and slight increase in incidence of death in the first few days.

The usual thrombolytic tPA therapy is alteplase 0.9 mg/kg up to 90 mg IV over 1 hour, with 10% of the dose given as an initial bolus¹ or tenecteplase. Withhold aspirin for 24 hours.

Note: Avoid steroids, mannitol, haemodilution and anticoagulation in acute stroke.⁴

Transient ischaemic attacks

Clinical features

• Sudden onset and short duration (<60 minutes)

• Usually complete clinical recovery in less than 24 hours

• Consciousness usually preserved

• Ninety per cent usually in anterior circulation

• Carotid TIAs—unilateral features

• Vertebrobasilar TIAs—often have bilateral or crossed features

A comparison of the main clinical features of carotid (anterior circulation) ischaemia and vertebrobasilar (posterior circulation) ischaemia is presented in FIGURE 130.1. The carotid circulation accounts for 80% of TIAs.

Differential diagnoses of TIAs are presented in TABLE 130.2.

Some ischaemic syndromes

• Transient monocular blindness (amaurosis fugax)

• Transient hemisphere attacks

• The ‘locked-in’ syndrome

• Vertebrobasilar:

  • – bilateral motor loss

  • – crossed sensory and motor loss

  • – diplopia

  • – bilateral blurring or blindness

Amaurosis fugax

This is the sudden transient loss of vision in one eye (like a ‘curtain or shade’ coming from above or below) due to the passage of an embolus through the retinal vessels from ipsilateral carotid vessel disease. It is a feature of a TIA in the carotid artery circulation and is often the first clinical evidence of carotid stenosis.⁵ About 20% of all TIAs present as amaurosis fugax.⁶ Amaurosis fugax may forewarn of the development of hemiparesis or blindness and should be considered a matter for urgent attention and rectification. Give aspirin immediately. Carotid endarterectomy may be required for high grade stenosis.

Differential diagnosis of transient amaurosis fugax

• thromboembolic phenomena

• vasospasm

• temporal arteritis

• blood—sickle cell, polycythaemia

• retinal—haemorrhage, venous thrombosis, detachment

• optic neuritis

• vitreous floaters

Transient hemisphere attack (usually middle cerebral artery)

• Affects motor or sensory or both

• Usually face and arm (more than leg)

• Dysphasia common

The ‘locked-in’ syndrome

In this syndrome, which may be transient or persistent, patients remain conscious and aware of their dilemma but are unable to speak or move the limbs, particularly the arms. It may be possible to communicate with patients using eye responses to commands. The cause is invariably a lesion in the brain stem.

Significance of TIAs

• Five years after a TIA, 22–51% (average 1 in 3) patients (without treatment) will have a stroke.^5,7 This figure may be higher for those with ipsilateral high-grade (70% or more) carotid stenosis.

• The highest risk is in the first 6 months.

• A carotid artery TIA has more serious prognostic significance. Such patients are at high risk of developing a stroke that is potentially preventable.

• Referral for investigation is appropriate.

• All patients should have a carotid duplex Doppler ultrasound and CT scan or MRI at presentation.

• Cardiac status should be addressed because of an association with myocardial infarction.

Investigations⁸

• A CT scan, 12–lead ECG and carotid imaging are essential investigations in the first hours of a suspected TIA

• Blood tests, echocardiography, MRI and Holter or bedside cardiac monitoring are likely to improve diagnosis

• Carotid duplex Doppler ultrasound for carotid territory symptoms

• Transoesophageal echocardiography

Management

• All high-risk patients admitted to a stroke unit or specialist TIA clinic: urgent attention for atrial fibrillation and carotid artery stenosis

• Aim to minimise the risk of a major stroke

• Determine cause and correct it (if possible)

• Early neurorehabilitation

• Advise cessation of smoking and treat hypertension (if applicable)

• Anti-platelet therapy (especially for carotid ischaemia):

  • aspirin 100–300 mg (o) daily (gives 30% protection from stroke or death after TIA)⁹

  • or

  • clopidogrel 75 mg (o) daily (or clopidogrel + aspirin)

  • or

  • dipyridamole CR + aspirin 200 mg/25 mg (o) bd (shows better outcomes than aspirin alone)¹⁰

  • or

  • ticlopidine (only if others unsuitable)

Antiplatelet therapy reduces the relative risk of stroke, myocardial infarction or vascular death by 22% (95% confidence interval 14–30%) in people with an ischaemic stroke or TIA due to arterial disease, compared with no treatment.²

• Anticoagulation therapy: warfarin:

  • – for vertebrobasilar ischaemia (with increasing frequency of TIAs)

  • – for failed anti-platelet therapy

  • – use direct oral anticoagulants (DOACs) for non-valvular atrial fibrillation >65 years of age

• Carotid endarterectomy has been proven to have a place in the management of carotid artery stenosis; the decision depends on the expertise of the unit. There is no evidence that surgery is appropriate for asymptomatic patients, nor for symptomatic patients with a stenosis less than 50%. Symptomatic patients benefit from surgery particularly for stenoses greater than 70%.^11,12 If the stenosis is >90%, refer immediately. Greater than 75% stenosis is associated with a 2% per annum rate of ipsilateral ischaemic stroke.¹

• Percutaneous transluminal angioplasty (stenting). Carotid artery stenting for the treatment and prevention of stroke should be restricted to those who are unsuitable for carotid endarterectomy.¹¹

Atrial fibrillation^1,13

• The main source of cardio–embolic infarction

• Increased with risk factors—hypertension, previous embolism and recent CHF (previous 3 months)

• With non-valvular AF, annual risk of CVA is 2.5% (no risk factors) to 17.6% (2 + risk factors)

• Risk of stroke about 6 times that of other people

• Intermittent AF can also be a risk

Management

• People with AF aged under 65 with no other risk factors do not require anticoagulant therapy.¹⁴

• Valvular disease: warfarin—target INR 2–3

• Non-valvular AF: calculate the risk-benefit ratio for anticoagulant therapy.

• Do not offer aspirin monotherapy solely for stroke prevention to people with AF.¹⁴

Selecting antithrombotic therapy in non-valvular AF is assisted by the CHADS₂ index, a validated tool (see TABLE 130.3). Many guidelines use a variation, the CHA₂DS₂-VASc score.

Cerebral venous thrombosis²

This rare cause of stroke may present as an acute or chronic cerebrovascular disorder. It should be suspected particularly in women in the postpartum period presenting with severe headache or focal neurological defects. Diagnosis is by MRI. In the acute phase, treatment is by anticoagulation with heparin followed by warfarin for approximately 6 months.

• Bruit in neck

• TIAs if diagnosis uncertain

• Crescendo TIAs (two or more in 1 week and longer lasting)

• Internal carotid artery symptoms

• Hemispheric stroke

• Prior to major vascular surgery (e.g. CABG)

Stroke in children is relatively uncommon. Causes include paradoxical embolus (e.g. PFO), cerebral vasculopathy (e.g. vasculitis), arterial dissection and metabolic disease. The most common clinical presentation of stroke in childhood is acute hemiparesis due to involvement of the carotid distribution.¹ Investigation includes immediate brain MRI or CT scan, transthoracic echocardiography, thrombophilia factors (e.g. V Leiden) and urine homocysteine. Consider also sickle-cell disease. Initial treatment within 48 hours and after imaging is aspirin 2–5 mg/kg up to 300 mg orally daily.

• Refer immediately to a stroke unit

• Suspicion of SAH

• Carotid artery stenosis on carotid duplex Doppler ultrasound scan

• Cerebellar haemorrhage on CT scan

• Stroke in a young patient <50 years (consider PFO and other, less common causes)

Proven strategies

Three proven strategies to improve outcome of acute stroke (level I evidence):

• management in a stroke unit

• giving IV tPA within 3 hours of ischaemic stroke

• giving antiplatelet agents ASAP and within 48 hours of ischaemic stroke

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Stroke

National Stroke Foundation, Australia. Clinical Guidelines for Stroke Management, 2013. <www.strokefoundation.com.au>

European Society of Cardiology Guidelines <www.escardio.org>