Stroke

Ischaemic Stroke

This refers to brain ischaemia that results in neurological damage lasting > 24 hours.

It occurs due to occlusion of an artery which reduces blood flow to the brain.

Embolic

This is where a clot breaks off and occludes a part of the cerebral circulation.

The most frequent source of emboli are clots dislodged from the left side of the heart, in patients with atrial fibrillation. These often block the middle cerebral artery (MCA).

Emboli can cause single arterial blockage or ‘showers’ to multiple arteries and arterial distributions.

Thrombotic

This is a stroke due to a rupture of an atherosclerotic plaque, commonly in the MCA.

Lacunar stroke

This is a stroke where there is occlusion of a single small perforating artery supplying subcortical areas.

It is usually secondary to arteriosclerosis from hypertension, causing small areas of infarction.

Risk factors

Hypertension

Smoking

Diabetes

Hyperlipidaemia

Atrial fibrillation

Hypercoagubility states

Symptoms

The Oxfordshire/Bamford stroke classification identifies 3 key features:

Unilateral hemiparesis or hemisensory deficit

Homonymous hemianopia

Higher order cerebral dysfunction, e.g., dysphasia, neglect

Vascular Territories and Associated Symptoms

Anterior circulation

This comprises of the anterior and middle cerebral artery.

A total anterior circulation stroke (TACS) gives all three of the above.

A partial anterior circulation stroke (PACS) gives two out of three of the above.

In an anterior cerebral artery stroke, the legs are affected more than the arms, due to the somatotropic map of the brain.

Posterior cerebral artery

This leads to a contralateral homonymous hemianopia with macular sparing and cerebellar symptoms.

Lacunar stroke

This can cause one of the following: sensory, motor or sensorimotor deficit, or ataxic hemiparesis.

Basilar artery

An occlusion of the basilar artery can give rise to locked-in syndrome.

Posterior cerebral artery branch to midbrain (Weber syndrome)

Ipsilateral oculomotor palsy, with contralateral weakness of arms and legs

Posterior inferior cerebellar artery (Wallenberg syndrome)

Cross-body sensory deficit: ipsilaterally face and contralaterally on the limbs

Key tests

Blood glucose reading to exclude hypoglycaemia as the cause

Non-contrast CT immediately to exclude haemorrhage (this can also identify gross ischaemic changes after a few hours and dense vessels suggestive of a thrombus)

Management

If haemorrhage has been ruled out, then it depends on the timing:

If within 4.5 hours of onset, arrange for thrombolysis (e.g., with alteplase)

Thrombectomy may be available in some cases (e.g., if symptom onset is within 6 hours of presentation and confirmed occlusion of the anterior circulation)

If later/other options unavailable, loading dose of 300 mg aspirin (if on anticoagulation, this is usually held for 14 days while the patient is on aspirin 300 mg).

Secondary prevention

Antiplatelet therapy e.g., clopidogrel; if contraindicated, aspirin and dipyridamole

Atorvastatin started in all regardless of cholesterol levels

Optimise blood pressure

If patient has atrial fibrillation, anticoagulation is started after 2 weeks to reduce the bleeding risk. A 72-hour heart monitor can be performed if no AF is seen on the ECG.

Carotid endarterectomy is recommended if the stroke/TIA is in the anterior circulation area, and there is ipsilateral carotid stenosis > 70% on carotid doppler and angiography

Transient Ischaemic Attack

This is an ischaemic event with the same symptoms as a stroke that last < 24 hours.

Without intervention, patients are at high risk of having a stroke.

Driving is prohibited until they have seen a specialist.

Key tests

MRI scan of brain is usually normal

Carotid doppler to look for carotid stenosis and angiography if stenosis seen

As for stroke, lipid profile, ECG (and 72-hour tape if no AF seen)

Management

Patients should be seen within 24 hours and offered aspirin 300 mg

Antiplatelet – clopidogrel lifelong

Statin to lower of cholesterol

Blood pressure management

Lifestyle factors

ABCD2 Score

Risk Factors

Points

Age

≥60

1

Blood Pressure

Systolic ≥140mm Hg OR Diastolic ≥90mm Hg

1

Clinical Features

Unilateral weakness with or without speech impairment
OR Speech impairment without unilateral weakness

2
1

Duration

TIA duration ≥60 mins
OR TIA duration 10-59 mins

2
1

Diabetes

 1
Total Score between 0-7

Haemorrhagic Strokes

Subarachnoid haemorrhage (SAH)

This is a bleed into the subarachnoid space.

It damages the brain through tissue hypoxia and raised intracranial pressure.

It can be spontaneous or secondary to trauma to the head e.g., road traffic accident

Subarachnoid haemorrhage

Risk factors

Hypertension, smoking

Arteriovenous malformation

Berry aneurysms (associated with polycystic kidneys)

Marfan syndrome

Symptoms

Sudden onset severe headache (like a thunderclap, in occipital region)

Vomiting, seizures, reduced consciousness

Meningism – photophobia and neck stiffness

Cheyne-Stokes breathing – deeper, then shallower with apnoea, occurs in cycles

Kernig’s sign (takes 6 hours to develop), defined as an inability to extend the knee when patient is supine and the hip/knee is flexed. This is caused by irritation to the motor nerves passing through the inflamed meninges under tension.

Complications

Rebleeding

Hyponatreamia (due to SIADH)

Hydrocephalus

Arterial vasospasm – cerebral arteries constrict causing secondary brain ischaemia

Key tests

1st line is non-contrast CT

Lumbar puncture if CT is negative, performed at least 12 hours after headache onset to look for xanthochromia (RBC breakdown in CSF)

If positive, angiography can be performed to identify surgical target

Management

Refer to neurosurgery – options include endovascular coiling/clipping

Give nimodipine to prevent artery vasospasm and reverse anticoagulation

Intracerebral Haemorrhage (ICH)

This is a bleed within the brain tissue or ventricles.

It is associated with a Charcot-Bouchard microaneurysm of the striate vessels.

The main risk factor is hypertension, which can be secondary to factors like hyperaldosteronism, smoking and diabetes.

Symptoms

Similar to SAH, e.g., headache, nausea, vomiting, low consciousness

Localising symptoms depending on area affected, e.g., hemiplegia

Key tests

Same as SAH (CT head is first line)

Management

Rapid correction of blood pressure (range 140–160 mm Hg) and clotting

Refer to neurosurgery – may require surgery (e.g., craniotomy or burr hole) if reduced conscious level and/or brain herniation present

Intracranial Venous Thrombosis

This is thrombosis of the cerebral veins in the sinuses which leads to cerebral infarction.

This usually occurs within one of the dural venous sinuses which are responsible for the venous drainage of the brain.

Risk factors

Hypercoagulable states – pregnancy, malignancy, SLE

Head injury, dehydration

Symptoms

Can be sudden onset, with headache, nausea and vomiting

Seizures

Hemipgeia

Cranial nerve palsies

Key tests

CT head to exclude subarachnoid haemorrhage

Thrombophilia screen blood test

CT/MRI venogram is the diagnostic test

Management

Anticoagulation with heparin/LMWH then warfarin

If deterioration, may require endovascular thrombolysis 

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