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Path Intro - Stroke

Terms in this set (106)

What is hypoxia?

An oxygen deficiency which causes cell injury by reducing aerobic oxidative respiration

What is ischaemia?

Reduced tissue blood flow

What is an infarct(ion)?

A localised area of ischaemic tissue necrosis (death) - usually coagulative necrosis

What is liquefactive necrosis?

Necrosis characterised by digestion of dead tissue into a liquid mass (unlike coagulative necrosis where tissue is preserved)

This is the type of hypoxic ischaemic necrosis that occurs in the....?

Stroke/CVA is a clinical term that refers to cerebrovascular diseases including what?

- Those that cause hypoxic ischaemic infarction of the brain (ischaemic stroke)

- Intracerebral/intraparenchymal and subarachnoid haemorrhages (haemorrhagic stroke)

Stroke is the 3rd largest killer in NZ (about 2500 people every year). Around 10% of stroke deaths occur in people....?

What are the most common types of ischaemic stroke?

- Global cerebral ischaemia (hypoxic ischaemic encephalopathy)

- Focal cerebral ischaemia (ischaemic infarction) - caused by thrombosis or embolism

What are some common causes of haemorrhagic stroke?

- Hypertensive intraparenchymal haemorrhage
- Rupture aneurysm (subarachnoid haemorrhage)

Here we see the different types of stroke:

First we are going to look at global cerebral ischaemia - this occurs when there is a generalised decrease in cerebral perfusion, such as with what three things?

- Cardiac arrest
- Shock
- Severe hypotension

Generalised hypoxia, as in what, can have the same effect?

Severe respiratory depression

The clinical outcome depends on the severity of the insult, ranging from reversible mild injury to what?

Severe generalised neuronal death leading to brain death

Some areas of the brain are more vulnerable to ischaemic injuries than others, including what ones?

- Hippocampus
- Purkinje cells of the cerebellum
- the "watershed" areas

Border Zone, or "watershed" areas lie where?

Between arterial perfusion territories (ie at the most distal reaches of the arterial blood supply)

Here we see a ACA-MCA watershed infarct - what can you see?

Tissue necrosis and breakdown

If we now look at focal cerebral ischaemia/ischaemic infarcts, obstruction of blood supply to a localised area of the brain for a long enough period of time can cause ischaemic infarction. The infarcts may be the result of occlusion of what?

- Large vessels (most commonly the Middle cerebral artery)

- Small penetrating vessels (those supplying the basal ganglia, thalamus and internal capsule)

Vascular occlusion may be the result of what or what?

- Embolism to the brain (usually from a thrombus = thromboembolism)

OR

- Thrombosis of cerebral vessels due to atherosclerosis

Sources of emboli (thromboemboli) to the brain include what three?

- The heart
- Aorta and carotid arteries
- Paradoxical emboli

What are the three possibilities of thromboemboli from the heart?

- Mural thrombus complicating an MI
- Thrombosis complicating AF
- Thrombosis complicating valvular diseases

In terms of the aorta and carotid arteries, this refers to what?

Thrombosis developing over atheromatous plaques (tiny emboli lead to TIAs or ministrokes)

Paradoxical emboli can occur, in which thromboemboli from the venous circulation may do what?

Pass through a cardiac septal defect (such as a patent foramen ovale) into the arterial circulation and embolise to the brain

What are some other forms of embolism that exist?

- Air embolism
- Fat embolism
- Amniotic fluid embolism

In terms of ischaemic infarcts, there are two types of infarcts, based on presence of what?

Haemorrhage WITHIN the infarct

What are these two types?

1) Haemorrhagic (red) infarct
2) Non-haemorrhagic (pale, bland) infarct

A haemorrhagic (red) infarct is typically associated with what?

It's characterised by what?

Multiple, sometimes confluent, petechial haemorrhages

Haemorrhage in this is due to reperfusion of damaged tissue through what?

- Collateral circulation
- Or following fibrinolysis of the thromboembolic material in the occluded vessel, leakage of blood through necrotic vessels occurs

Non-haemorrhagic (pale, bland) infarcts are usually associated with what?

here we see a haemorrhagic infarct showing....?

Petechial haemorrhages

Management differs greatly for the two types of infarct - what is used in thrombotic cases?

Thrombolytic therapy (this is usually administered up to 6 hours)

It's contraindicated however in....?

Haemorrhagic infarcts

An area termed what lies around the ischaemic area, and is potentially reversible if the circulation is restored?

Clinical presentation and functional outcome of an infarct depends on its...?

Size and location

Blood supply of the brain:

Here we can see the primary motor and primary somatosensory areas:

The upper halves of the anterior and posterior limbs of the internal capsule are supplied by what?

The MCA

On this diagram we can see where the fibres from the different areas go through.

In terms of gross appearances, an infarct that has occurred from 0-6 hours before a patient's death is almost always....?

Undetectable macroscopically (unless it's haemorrhagic!)

By 48 hours, there is what?

- Blurring of the grey/white matter interface

- The infarct is pale, soft, swollen, and ill-defined (this is due to extensive vasogenic oedema due to the disruption of the BBB and passage of fluid into the extracellular space)

From 2-10 days, the area of the brain infarct becomes....?

Gelatinous and friable

The infarct now has a....?

well-defined border

From 10 days to 3 weeks, what happens grossly?

The tissue breaks down and liquefies, leaving cystic spaces (fluid-cavities), lined by dark grey tissue (gliosis)

Why do we get brain oedema following an infarct? This is because tissue necrosis triggers....?

Inflammation, and loss of structural integrity of blood vessels due to infarction, lead to what?

Disruption of the BBB

The result is what?

An increase in the vascular permeability and extravasation of fluid

What do we call this?

Vasogenic oedema

Over time, oedema may be severe enough to cause....?

Raised ICP and brain herniation

In terms of clinical imaging to detect oedema in acute ishcaemic stroke, on the day of the stroke, CT....?

Fails to reveal significant damage

On the same day however, diffusion-weighted MRI shows what?

Areas of oedema (water is white like in a T2 MRI) - in part of the right middle cerebral artery distribution

Three days later, what shows up in CT images?

Oedema (water) shows up as hypodense

Here we see the gross appearance of a weeks-old infarct in the right MCA territory, showing extensive tissue breakdown. Note thwat on the side of the infarct?

Here we see a weeks-old extensive left MCA territory infarct (especially involving the basal ganglia) - with massive...?

Left to right midline shift

Here we see a partially liquefied infarct of the frontal lobe showing what?

Liquefactive necrosis with formation of cystic spaces

Here we see a months/years old infarct with a large....?

Defect/cystic space (surrounded by gliosis)

Now in terms of microscopic appearances of ischaemic infarcts, histological appearance varies with what?

The age of the lesion

Early (12-24 hours): Neuronal injury is manifested by what two features?

- Cytoplasmic eosinophilia, and
- Nuclear pyknosis

So called "red, dead neurons" - this is the main change seen in vulnerable areas of the brain in Global Cerebral Ischaemia.

At this point (12-24 hours) what else are evident?

Neutrophilic infiltrates (inflammation triggered by tissue necrosis) - this then subsides after about 48 hours.

What do you see at the subacute stage (24 hours - 2 weeks)?

- Tissue necrosis
- Macrophage infiltrates
- Vascular proliferation and
- Starting gliosis

What do we see during the repair stage (2 weeks onwards)?

Removal of necrotic tissue by macrophages, leaving a cystic space surrounded by gliosis.

Haemorrhagic infarct will, in addition to the above time-related changes, show what?

Blood extravasation and resorption

Here we see normal brain histology (grey and white matter):

Here we see the early/acute phase (red dead neurons) - this change is what will be seen in vulnerable areas of the brain in what?

Global cerebral ischaemia

Here we see the subacute stage - where we can see what?

- Macrophage infiltrates (foamy macrophages inside infarct - containing fat from the breakdown of brain tissue)

- Surrounding gliosis (proliferated astrocytes - both plump and small)

Here we see the chronic phase - a cavity surrounded by gliosis. Years old infarcts will persist as a....?

Cystic cavity that would be lined by macrophages (haemosiderin-laden in the case of haemorrhagic infarcts) - surrounded by a rim of reactive gliosis

Gliosis is the indicator of what, regardless of aetiology?

Gliosis is characterised by what?

Hypertrophy and hyperplasia of mainly astrocyes

Astrocytes are the main "glial" cells (these are cells that have supporting/connective tissue function) in the CNS - hence the alternative term for this process, ...?

Astrocytes derive their name from their....?

Star-shaped appearance

Astrocytic cell processes form what?

A dense web that surrounds lesions in the CNS

Here we can see stellate astrocytes and their....?

Cytoplasmic processes

Gliosis surrounds lesions in the brain like a...?

Now we will look at hypertensive cerebrovascular disease: Hypertension affects what?

The deep penetrating arteries and arterioles that supply the basal ganglia and hemispheric white matter, as well as the brainstem

In chronic hypertension, these cerebral arterioles develop what?

Hyaline arteriolosclerosis - with thickening (yet weakening) of their walls + narrowing of their lumens

This predisposes the cerebral arterioles to what?

Vascular occlusion and/or rupture

Hyaline arteriolosclerosis is chased by plasma protein leakage across injured endothelial cells and what else?

Extracellular matrix deposition by vascular smooth muscle cells

This is all in response to what?

To the dynamic stresses of hypertension

Hypertension also potentiates what, thus predisposing to thrombosis?

Cerebral atherosclerosis

Rupture of larger-calibre penetrating vessels leads to large...?

Intracerebral (intraparenchymal) haemorrhages

Rupture of smaller-calibre penetrating vessels can lead to the development of what?

Small, slit haemorrhages

Vascular occlusion leads to small infarcts called what?

Lacunar infarcts (lacunae meaning small, lake-like cavities)

Hypertension can also lead to minute what?

Aneurysms (due to weakening of the vessel walls)

These are called what?

Charcot-Bouchard micro-aneurysms

These may be the site of rupture and bleeding in the...?

Basal ganglia (not to be confused with saccular "berry" aneurysms of larger intracranial vessels in the subarachnoid space)

Here we can see lacunar infarcts:

What is the most common cause of non-traumatic deep brain parenchymal haemorrhages?

Hypertensive intraparenchymal haemorrhage commonly involves what structures (in descending order)?

- Basal ganglia (usually the putamen in 50-60% of cases)
- Thalamus
- Pons
- Cerebellum

Here we can see a hypertensive intracerebral haemorrhage - this is a hypertensive bleed involving the....?

Basal ganglia (mainly the putamen) - note also the mmidline shift and ventricular compression

Here we can see a hypertensive intraparenchymal haemorrhage/bleed where?

In the right thalamic lesion with extension into the ventricles

Now looking at duret haemorrhages, these are linear haemorrhages seen where and when?

Seen in the midline of the midbrain and pons in cases of uncal herniation

Duret haemorrhages are thought to be the result of what?

Tearing of penetrating veins and arteries supplying the upper brainstem, during the progression of transtentorial/uncal herniation

Here we can see Duret haemorrhages:

Now looking at subarachnoid haemorrhage: The most frequent cause (85% of cases) of subarachnoid haemorrhage is what?

Non-traumatic (spontaneous) rupture of a saccular "berry" aneurysm in a cerebral artery

The most common symptom of a subarachnoid haemorrhage is what?

Severe "thunderclap" headache of sudden onset

There are usually also signs of what?

Meningeal irritation:
- Photophobia
- Positive Kernig's (and/or Brudzinski's) signs
- Neck stiffness
- Headache

Subarachnoid haemorrhage also shows the signs and symptoms of...?

The immediate mortality of aneurysmal subarachnoid haemorrhage (SAH) is about 30%. Survivors have a recurrence (rebleed) rate of what?

- About 40% in the first 4 weeks
- 3% annually thereafter

SAH may also result from what other causes?

- Extension of a traumatic haematoma
- Rupture of a hypertensive intracerebral haemorrhage into the ventricular system
- Vascular malformations
- Haematologic disturbances
- Brain tumours

Saccular "berry" aneurysms are found in about how much of the population?

Multiple aneurysms are seen in 20-30% of cases. These aneurysms are thought to result from what?

Congenital defects in the arterial wall

They aren't present at birth but develop at a young age. They occur at....?

Arterial branching points

The common sites (and how common they are at each site) are depicted in this diagram:

Note that what is also considered a risk factor for developing berry aneurysms and increases the likelihood of rupture?

Here we can see a dissected Circle of Willis showing 3 berry aneurysms (which would lead to subarachnoid haemorrhage):

Here we can see a rupture berry aneurysm in the base of the brain:

Here we can see another image of the base of a brain showing a what from a rupture Berry Aneurysm?

Subarachnoid haemorrhage

Here we can see a subarachnoid haemorrhage on CT - we can see what?

Blood filling the basal CSF cisterns (due to the subarachnoid haemorrhage) - this is the "Dancing Man" sign

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