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MD1 Neuroscience > Stroke > Flashcards

Stroke Flashcards

1
Q

What is the clinical definition of a stroke?

A

Focal or global neurologic deficit development related to a vascular event

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2
Q

What are the 3 different pathalogic processes involved in stroke?

A

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

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3
Q

What are the risk factors for cerebral infarction?

A

Aging

Hypertension

Cardiac disease (e.g. atrial fibrillation)

Hyperlipidaemia

Diabetes mellitus

Hypercoagulable states, e.g. antiphospholipid antibody syndrome

Smoking, obesity

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4
Q

What is cerebral infarction?

A

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

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5
Q

What are the 3 possible causes of cerebral infarction?

A

Pump failure

Narrowed vessel lumen

Embolus

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6
Q

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

A

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

Thrombosis

Hypertensive vessel thickening, diabetes

Amyloid angiopathy

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7
Q

What is large artery occlusion most commonly due to?

A

Embolus

Thrombus less common

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8
Q

What is small vessel occlusion most commonly due to?

A

Thrombosis (less common embolus)

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9
Q

What is venous occlusion commonly due to?

A

Thrombus

Never embolus (can’t pass into venous circulation)

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10
Q

How can heart vegetations give rise to cerebral infarction?

A

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.

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11
Q

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

A

Most thrombi occur in venous circulation.

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

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12
Q

What are the common sites of atherosclerosis?

A

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

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13
Q

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

A

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

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14
Q

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

A

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.

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15
Q

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

A

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

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16
Q

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

A

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

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17
Q

What happens to the brain hours after a cerebral infarct?

A

Cytotoxic oedema

Cells break down

Tissue accumulates fluid

Swelling and vasogenic oedema affecting neighbouring white matter

Brain starts to herniate

18
Q

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

A

It starts to disappear.

19
Q

What happens to neurons in cerebral infarction?

A

They die

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

20
Q

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

A

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
Q

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

A

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

The area is now a cystic space filled with CSF.

22
Q

What causes haemorrhagic cerebral infarction?

A
  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
Q

What is the most common small blood vessel infarct?

A

Small vessel hyaline arteriolosclerosis due to hypertension.

24
Q

What is the most common small blood vessel infarct?

A

Small vessel hyaline arteriolosclerosis due to hypertension.

25
Q

How does hypertensive small vessel disease cause cerebral infarction?

A

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

26
Q

What can small infarcts develop into?

A

Cysts

27
Q

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

A

Pneumonia, CV disease and pulmonary thromboembolism.

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

28
Q

What are the causes of intracerebral haemorrhage?

A

Hypertensive small vessel disease – most common

Congophilic [amyloid] angiopathy – second most common

Blood disorders

Tumour

Vasculitis

Vascular malformation

Drugs

29
Q

What is hypertensive haemorrhage characterised by?

A

Presence of small vessel disease

(hyaline arteriolosclerosis)

30
Q

What are the particular sites of predilection for hypertensive haemorrhage?

A

Basal ganglia/thalamus

Lobar white matter

Cerebellum

Pons

31
Q

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

A

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

32
Q

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

A

Hypertensive haemorrhage

33
Q

What is cerebral amyloid angiopathy?

A

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

34
Q

What is a common cause of multifocal synchronous haemorrhage?

A

Coagulopathy

Thrombocytopaenia

Leukaemia or multiple metastatic lesions which have become haemorrhagic

35
Q

How can arteriovenous malformation cause haemorrhagic infarction?

A

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
Q

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

A

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
Q

What are the risk factors for developing a saccular aneurysm?

A

Sex and age

Polycystic kidney disease

Coarctation of aorta

Type III collagen deficiency et al

Hypertension

Smoking/alcohol

38
Q

Where do saccular aneurysms generally occur?

A

At sites of congenital weakness at arterial bifurcations.

39
Q

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

A

Anterior circulation (much more often than posterior)

40
Q

What are the favoured sites of saccular aneurysms?

A

Bi/trifurcation of middle cerebral artery

Junction of ICA and posterior communicating artery

Anterior communicating artery

41
Q

What are the common sites of saccular aneurysm formation?

A

MCA bi-trifurcation

ACA/Ant communicating artery.

Distal ICA complex

42
Q

What are the potential complications of aneurysm rupture?

A

Subarachnoid haemorrhage [+/- intraparenchymal]

Cerebral oedema & raised ICP

Vasospasm and infarction

Ventricularobstruction - hydrocephalus

MD1 Neuroscience (23 decks)

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