MDG5204 Chap.10 Ischaemic Stroke: Mechanisms and Acute Treatment
Ischaemic Stroke: Mechanisms and Acute Treatment
A major cause of death and disability
The stroke lecture opens with its scale. Stroke is a leading cause of death and disability, its outcome depends on the size and site of the lesion, the window for saving tissue is narrow, and both recurrence and first strokes can be prevented.
The Singapore data the course presents show stroke as the fourth leading cause of death in 2008, with falling standardised mortality but rising hospital admissions, and a patient population in which hypertension and diabetes were common.
Definition and mechanisms
The WHO definition the course uses describes rapidly developing signs of a focal, occasionally global, loss of brain function that persist beyond 24 hours or end in death, where the only evident cause is vascular.
Strokes arise from arterial rupture, causing intraparenchymal or subarachnoid haemorrhage, or from arterial occlusion by atherothrombosis, atheroembolism, small artery disease or cardioembolism, causing ischaemia and infarction.
The phrase time is brain summarises the ischaemic cascade that follows occlusion.
Risk factors and localisation
Non-modifiable risk factors include older age, male sex, prothrombotic genetics and ethnicity; modifiable ones are led by atrial fibrillation, blood pressure, smoking, diabetes, alcohol and hyperlipidaemia.
The symptoms depend on which arterial territory is affected, so the course revises the circle of Willis and the territories of the anterior, middle and posterior cerebral arteries, the basilar and vertebral arteries and the cerebellar arteries.
Acute treatment
Management starts with an accurate diagnosis, and a brain scan comes first because haemorrhage contraindicates antithrombotic drugs and clinical scores separate haemorrhage from infarction only about 70% of the time.
Thrombolysis with streptokinase, urokinase or recombinant tissue plasminogen activator aims to restore flow, carries a risk of haemorrhage and works only in a narrow window of 3 hours, extended to 4.5. Neuroprotection has so far failed in trials, except for nimodipine in subarachnoid haemorrhage; volume expansion is ineffective and steroids are dangerous.
Preventing complications such as infection, aspiration and venous thrombosis is part of the treatment.
What this chapter covers
- 01
The burden of stroke in Singapore as the course presents it
- 02
The WHO definition and the transient ischaemic attack
- 03
Rupture against occlusion and the ischaemic cascade
- 04
Modifiable and non-modifiable risk factors
- 05
Arterial territories and the circle of Willis
- 06
Imaging first, thrombolysis within the window and failed neuroprotection
Worked example · free
Explaining why a thrombolytic can be the wrong drug
- 2State what a haemorrhage means for antithrombotic drugs.
- 2State how reliably clinical assessment separates the two.
- 1Conclude the order of decisions.
Key terms
- Ischaemic Stroke
- Stroke caused by arterial occlusion that deprives brain tissue of blood and leads to infarction.
- Haemorrhagic Stroke
- Stroke caused by arterial rupture, with bleeding into the brain or the subarachnoid space.
- Transient Ischaemic Attack
- A focal vascular disturbance of brain function that resolves without meeting the stroke definition.
- Thrombolysis
- Drug treatment that breaks down an occluding clot to restore blood flow.
- Neuroprotection
- Treatment aimed at halting the ischaemic cascade before brain cells die.
- Circle of Willis
- The ring of connected arteries at the base of the brain linking the carotid and vertebrobasilar supplies.
- Cardioembolism
- Occlusion of a brain artery by a clot formed in the heart, for example in atrial fibrillation.
Ischaemic Stroke: Mechanisms and Acute Treatment FAQ
What does time is brain mean in practice?
Once an artery is blocked, the ischaemic cascade progresses minute by minute and tissue that could be saved is lost. Treatment that restores flow, such as thrombolysis, is only offered within a narrow window of about 3 to 4.5 hours, so delay directly reduces what can be rescued.
Why have neuroprotective drugs not become standard stroke treatment?
Many have been tested and none has proven effective in patients, apart from nimodipine in subarachnoid haemorrhage; some trials were stopped because of side effects. The course links part of this failure to the gap between animal models and human stroke, which the next chapter examines.
Which risk factors for stroke can be changed?
Atrial fibrillation, high blood pressure, smoking, diabetes, alcohol, high blood lipids and a sedentary or obese lifestyle are the main modifiable ones, along with hormones, infections, drug use, carotid stenosis and some medications. Age, male sex, prothrombotic genetics and ethnicity cannot be changed.
Exam move
Learn the acute sequence as a short flow of decisions, scan, haemorrhage or not, time since onset, then treatment, and practise writing it from memory with one reason attached to each step.
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