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MD1 Neuroscience > Stroke > Flashcards

Flashcards in Stroke Deck (42)
1

What is the clinical definition of a stroke?

Focal or global neurologic deficit development related to a vascular event

2

What are the 3 different pathalogic processes involved in stroke?

Infarction (75%): death of tissue due to inadequate blood supply

Haemorrhage (20%): tissue injury due to the escape of blood from vessel(s)

Subarachnoid haemorrhage (5%): Escape of blood primarily into the subarachnoid space

3

What are the risk factors for cerebral infarction?

Aging

Hypertension

Cardiac disease (e.g. atrial fibrillation)

Hyperlipidaemia

Diabetes mellitus

Hypercoagulable states, e.g. antiphospholipid antibody syndrome

Smoking, obesity

4

What is cerebral infarction?

Necrosis of cerebral tissue in a vascular distribution due to vessel occlusion or severe hypoperfusion.

5

What are the 3 possible causes of cerebral infarction?

Pump failure

Narrowed vessel lumen

Embolus

6

What are the 4 ways a lumen can narrow leading to inadequate blood supply and cerebral infarction?

Atherosclerosis – due to a piece breaking off or from the narrowed vessel being plugged itself.

Thrombosis

Hypertensive vessel thickening, diabetes

Amyloid angiopathy

7

What is large artery occlusion most commonly due to?

Embolus

Thrombus less common

8

What is small vessel occlusion most commonly due to?

Thrombosis (less common embolus)

9

What is venous occlusion commonly due to?

Thrombus

Never embolus (can't pass into venous circulation)

10

How can heart vegetations give rise to cerebral infarction?

Valve vegetations in left heart due to non-bacterial thrombotic endocarditis occur when valve is abnormal, e.g. post-rheumatic fever.

Thrombus flicks off and travels to the brain.

11

How can a thrombus from the right side of the heart cause cerebral infarction?

Most thrombi occur in venous circulation.

Thrombus flicks through atrial septal defect (present in 1/3 population) and travels to brain on ventricular ejection.

12

What are the common sites of atherosclerosis?

Vertebral, basilar, internal carotid, terminal arteries and proximal cerebral arteries.

13

How can an abnormal configuration of the Circle of Willis be beneficial?

Because if there is an occlusion, blood can sometimes enter from the other side of the infarct, overcoming the deficit.

14

What are the 2 ways in which atherosclerosis can lead to cerebral infarct?

The lumen becomes progressively smaller, leading to a greater propensity for thrombus to develop.

Or, the atherosclerosis can ulcerate and a thrombus will develop on the surface of the ulcerated plaque.

15

What operation can be performed to prevent ulcerated or stenotic atherosclerosis from causing cerebral infarction?

Stripping out of the thickened intima and some of the media of the carotid artery and removal of the ulcerated plaque or stenosing atherosclerosis.

16

What is the macroscopic appearance of a region of cerebral infarct within hours after the infarct?

Relatively normal, hence why CT scans aren't particularly sensitive and MRI must be used (more sensitive).

17

What happens to the brain hours after a cerebral infarct?

Cytotoxic oedema

Cells break down

Tissue accumulates fluid

Swelling and vasogenic oedema affecting neighbouring white matter

Brain starts to herniate

18

What happens to the demarcation between cortex and white matter in cerebral infarct?

It starts to disappear.

19

What happens to neurons in cerebral infarction?

They die

Become hypereosinophilic and then shrink down, becoming much smaller until the nucleus disappears altogether.

20

What happens to a region of cerebral infarct days to weeks after the injury?

Swelling subsides, brain parenchyma breaks down.

Cerebral tissue has become necrotic, macrophages start removing dead tissue.

Liquefactive necrosis occurs, resulting in evolving cystic change.

21

What happens to a region of cerebral infarct months to years after the injury?

There's no more tissue in the region at all.

The area is now a cystic space filled with CSF.

22

What causes haemorrhagic cerebral infarction?

  1. Blood vessels in the area of infarction die.
  2. Reperfusion of the site
  3. Vessel wall can no longer sustain the pressure of blood.
  4. Haemorrhage

23

What is the most common small blood vessel infarct?

Small vessel hyaline arteriolosclerosis due to hypertension.

24

What is the most common small blood vessel infarct?

Small vessel hyaline arteriolosclerosis due to hypertension.

25

How does hypertensive small vessel disease cause cerebral infarction?

Can cause narrowing of the vessel followed by thrombus or ballooning of the weak vessel, causing small local aneurysm then rupture

26

What can small infarcts develop into?

Cysts

27

What is the most common reason people with cerebral infarcts die?

Pneumonia, CV disease and pulmonary thromboembolism.

Complications of the infarct and pre-existing risk factors  are most likely to cause death.

28

What are the causes of intracerebral haemorrhage?

Hypertensive small vessel disease – most common

Congophilic [amyloid] angiopathy – second most common

Blood disorders

Tumour

Vasculitis

Vascular malformation

Drugs

29

What is hypertensive haemorrhage characterised by?

Presence of small vessel disease

(hyaline arteriolosclerosis)

30

What are the particular sites of predilection for hypertensive haemorrhage?

Basal ganglia/thalamus

Lobar white matter

Cerebellum

Pons

31

Why can hypertensive haemorrhage in the cerebellum be a neurosurgical emergency?

Because it can cause acute obstruction of the 4th ventricle, leading to raised ICP

32

What are superficial cortex and white matter not commonly associated with?

Hypertensive haemorrhage

33

What is cerebral amyloid angiopathy?

Deposition of amyloid-beta in walls of superficial supratentorial blood vessels causing multiple superficial haemorrhages due to rupture (occlusion less common)

34

What is a common cause of multifocal synchronous haemorrhage?

Coagulopathy

Thrombocytopaenia

Leukaemia or multiple metastatic lesions which have become haemorrhagic

35

How can arteriovenous malformation cause haemorrhagic infarction?

The arteries and veins are in unnatural relationships to one another, therefore high pressure blood can pass directly into venous vessels, bypassing the capillaries and leading to rupture.

36

What are the common causes of non-traumatic subarachnoid haemorrhage?

Rupture of saccular (Berry) aneurysm.

Rupture of other types of aneurysm

Mycotic (infective)

Atherosclerotic – atherosclerosis can (in some people) cause the vessels to dilate

Extension of intracerebral haemorrhage into subarachnoid space

37

What are the risk factors for developing a saccular aneurysm?

Sex and age

Polycystic kidney disease

Coarctation of aorta

Type III collagen deficiency et al

Hypertension

Smoking/alcohol

38

Where do saccular aneurysms generally occur?

At sites of congenital weakness at arterial bifurcations.

39

In which branch of the cerebral circulation do saccular aneurysms tend to occur most?

Anterior circulation (much more often than posterior)

40

What are the favoured sites of saccular aneurysms?

Bi/trifurcation of middle cerebral artery

Junction of ICA and posterior communicating artery

Anterior communicating artery

41

What are the common sites of saccular aneurysm formation?

MCA bi-trifurcation

ACA/Ant communicating artery.

Distal ICA complex

42

What are the potential complications of aneurysm rupture?

Subarachnoid haemorrhage [+/- intraparenchymal]

Cerebral oedema & raised ICP

Vasospasm and infarction

Ventricularobstruction - hydrocephalus