Stroke

Question 1

Transient ischaemic attack TIA: mini stroke

Answer 1

An acute focal neurological deficit caused by a temporary disruption to the blood supply. Signs and symptoms disappear within 24 hours.

Signs/ symptoms: weakness on one side- arm, leg, face, difficulty with speech, dizziness, vertigo etc. (same for stroke)

Question 2

Stroke aetiology: ischaemic stroke

Answer 2

Occluded blood vessels- 80% of strokes.
- atheroma and thrombosis
Most commonly caused by an atheroma and thrombus in a cerebral artery.
- embolism- most are thromboemboli and most are cardiogenic. Also arise from fat emboli, bacterial emboli etc.
- cryptogenic (unknown causes)

Consequences of IS:
Depends on- functional reserve (compare with kidney) and regenerative capacity, size of blockage, speed and duration of blockage

The circle of willis supplies collateral circulation the the brain. Sometimes the collateral vessels are not open, but they can open and provide blood flow if given time. Can stimulate angiogenesis in areas of Ischaemia, but takes time to become effective.

Question 3

Compare clinical effects of ischaemic strokes

Answer 3

Atheroma and thrombus may cause partial obstruction. Usually found in larger vessels, usually a gradual build up, may be warning signs, TIA

Emboli lodge is smaller cerebral vessels, can be multiple emboli and jnfarcts. Occlusion is usually complete. Occlusion is sudden, may haemorrhage later.

IS generally obstructs carotid artery and middle cerebral.

Question 4

Mechanisms of injury and progression of stroke

Answer 4

In the core area, cells die due to lack of blood supply, decreased O2, nutrients and Increased waste products can be toxic.
Penumbra- area peripheral to the Infarct. Cells here may still survive. In the penumbra, cells weaken due to decreased ability to maintain homeostasis, lack of oxygen in the tissue creates acidity, build up of waste products, cells in this area may die later.
Stroke progression from oedema and inflammation.

Question 5

Stroke aetiology: haemorrhagic

Answer 5

• intracerebral haemorrhage
  Smaller, penetrating arteries break, causing blessing into brain tissues. Approx 10-15%
  Caused by HT- causes formation of microaneurysms and high BP, causes the aneurysms to rupture. Clinical effects- immediate include pressure against brain tissue, loss of blood to brain, pressure caused more vessels esp veins to break. Delayed- oedema and inflammation.
• subarachnoid haemorrhage
  Most are form ruptured berry aneurysms- caused by genetics, familial aggregation. Berry aneurysms are prone to rupture esp if hypertensive, forming a subarachnoid haemorrhage. Clinical effects- immediate: loss of blood flow to brain, pressure against brain. Delayed- rebleed, cerebral vasospasm- reduced blood flow to brain. Can be treated by endovascular coiling.
  Others are from vascular inflammations, cocaine etc.

Question 6

Cause of death after strokes

Answer 6

Pneumonia

Cardiovascular- myocardial infarction, pulmonary embolism, septicaemia, transtentorial herniation

Question 7

Stroke/ cerebrovascular disease

Answer 7

An acute focal neurological deficit, caused by disruption to blood supply.
The disruption to blood supply is caused by diseased or malformed vessels.