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MHD2 Block 2 - Neuro > Cerebrovascular disease > Flashcards

Cerebrovascular disease Flashcards

1
Q

How long does it take for ischemia to cause irreversible brain damage?

A

6-8 minutes

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2
Q

List the CNS cells in order of susceptibility to ischemia from most sensitive to least sensitive

A

Neurons > oligodendrocytes > endothelial cells > astrocytes

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3
Q

What specific brain regions are particularly susceptible to ischemia?

A

Pyramidal neurons in CA1 hippocampus
Purkinje cells of the cerebellum
Cortical layers 3 & 5

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4
Q

What are the two broad categories of cerebrovascular disease?

A

Cerebral ischemia: can be global or focal

Intracranial hemorrhage: can be intraparenchymal or subarachnoid

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5
Q

What are the major etiologies of global cerebral ischemia?

A

Low perfusion (atherosclerosis)
Acute decrease in blood flow (cardiogenic shock)
Chronic hypoxia (anemia)
Repeated episodes of hypoglycemia (insulinoma)

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6
Q

What regions of the brain are affected by moderate global ischemia?

A

Watershed areas, which are the most distally perfused regions of the brain, which are the most vulnerable to infarction

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7
Q

What is the first histological change seen after global cerebral ischemia?

A

Red dead neurons: cytoplasmic eosinophilia, loss of Nissl substance and dark pyknotic nuclei

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8
Q

What is laminar necrosis?

A

The cerebral cortex layers 3 and 5 are susceptible to ischemia, resulting in ribbon-like laminar necrosis

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9
Q

What are the different types of focal ischemia?

A

Thrombotic, embolic, and small vessel

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10
Q

What is the etiology of thrombotic ischemic stroke?

A

Atherosclerotic plaque, most often at bifurcation of internal carotids (Flow is most turbulent at these points)

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11
Q

What is the etiology of embolic ischemic stroke?

A

Distant source of clot, most often from atrial fibrillation

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12
Q

Symptoms of a MCA ischemic infarct

A

Contralateral hemiparesis and hemisensory loss (lower face, upper extremity>lower extremity)
Contralateral visual field deficits

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13
Q

What is the difference between dominant and non-dominant hemispheric infarcts?

A

Dominant infarcts are associated with expressive aphasia

Nondominant are associated with neglect syndrome

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14
Q

What is the major gross difference between embolic and thrombotic infarcts?

A

Embolic cause red infarcts

Thrombotic cause pale infarcts

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15
Q

Describe how cerebral ischemic infarcts change grossly over time

A

6-48h: pale, swollen, indistinct border, blurred grey-white junction
2d-3wk: gelatinous, distinct border, liquefaction
>3wks: cystic, secondary degeneration

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16
Q

Describe how cerebral ischemic infarcts change microscopically over time

A 
6-12h: red neurons, pallor
1-3d: neutrophils
4-7d: macrophages
7-14d: vascular proliferation
>3wks: astrocytic gliosis, residual macrophages
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17
Q

Typical appearance of an embolic infarct

A

Most often MCA

Smaller than thrombotic, centered at junction between gray and white matter

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18
Q

Most common location of lacunar infarct

A

basal ganglia, thalamus, pons and subcortical white matter

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19
Q

What is the most common etiology of a hemorrhagic infarction?

A

Embolic

Embolus gets lysed resulting in secondary hemorrhagic infarction

20
Q

How are intracranial hemorrhages classified?

A

Based on location of bleed.
Above the arachnoid: epidural and subdural hematomas (usually from trauma)
Below the arachnoid: subarachnoid hemorrhage, parenchymal (usually from cerebrovascular disease)

21
Q

What brain regions are most often affected by hypertensive hemorrhages?

A

Putamen, thalamus, pons, cerebellum

This occurs due to rupture of pseudoaneurysms (Charcot-Bouchard)

22
Q

What is the most common cause of non-traumatic spontaneous subarachnoid hemorrhage?

A

Rupture of a berry aneurysm

Trauma is the most common cause overall

23
Q

Define xanthochromia

A

Yellow hue of CSF due to breakdown of bilirubin

24
Q

Where are Berry aneurysms most often found?

A

Most often in the anterior communicating artery

25
Q

What is a Duret hemorrhage?

A

Herniation of the medial temporal lobe compresses the pons leading to ischemia of perforating arterioles

26
Q

What is an epidural hematoma?

A

Blood between the dura and the skull due to fracture of the temporal bone and rupture of middle meningeal artery.

On CT: lens shaped lesion

27
Q

What is a subdural hematoma?

A

Blood underneath the dura secondary to the tearing of bridging veins between the dura and arachnoid, usually due to trauma more often in elderly.

On CT: crescent shaped lesion

28
Q

What are the three major types of brain herniation and their associated region?

A

Tonsillar: cerebellar tonsils through foramen magnum
Subfalcine: cingulate gyrus under falx cerebri
Uncal: uncus under tentorium cerebelli

29
Q

Clinical presentation of a tonsilar herniation

A

Cardiopulmonary arrest due to compression of the brainstem

30
Q

Clinical presentation of a subfalcine herniation

A

Can cause infarction due to compression of the ACA

31
Q

Clinical presentation of an uncal herniation

A

Compression of CN III causes dilated pupil, eye down and out
Compression of PCA can cause occipital infarction
Rupture of the paramedian artery can cause a Duret hemorrhage

32
Q

What are the two major subtypes of stroke?

A

Ischemic (most strokes)

Hemorrhagic

33
Q

Risk factors for cerebrovascular disease

A

Same as atherosclerosis: hypertension, heart disease, smoking, DM, hyperlipidemia, family history, obesity lifestyle, excessive EtOH, aging

34
Q

How does the body respond to gradual occlusion of a cerebral artery?

A

Collateral blood flows through the circle of Willis allow for blood to bypass the occlusion and deliver adequate blood flow to endangered areas of the brain.

If collaterals do not form, ischemic infarction will occur

35
Q

What is a transient ischemic attack (TIA)?

A

Reversible focal neurological deficit resolving within 24 hrs

36
Q

What is amaurosis fugax?

A

Monocular blindness caused by a TIA of the carotid artery

37
Q

Difference in likely etiologies of large vessel vs small vessel disease?

A

Large vessel disease can be caused by local thrombosis or an embolus. Small vessel disease is not caused by emboli, but can be due to thrombosis.

38
Q

3 Major steps of evaluation of TIA or ischemic infarction

A

1) Is there a lesion within symptomatic artery?
2) Is there a cardiac source of emboli?
3) Is there a hypercoagulable state?

39
Q

Preferred imaging modality for TIA or ischemic infarction

A

MRI (CT is 2nd choice)

To rule out tumor, hemorrhage, abscess, encephalitis

40
Q

Typical etiology of lacunar infarction

A

Thrombosis of atherosclerotic plaque due to hypertension, diabetes or old age
Not caused by emboli

41
Q

Presentation of a patient with lacunar infarction of the internal capsule

A

Pure motor defect: hemiplegia, ataxic hemiparesis, clumsy hand dysarthria

42
Q

Presentation of a patient with lacunar infarction of thalamus

A

Pure sensory stroke

43
Q

Treatment of acute cerebral infarction

A

If within 3 hours, IV tPA
If no tPA, aspirin can be used
Control BP
Prevent/treat complications

44
Q

How are TIA/strokes prevented?

A

Controlling risk factors
Surgically: carotid endarterectomy
Anticoagulants
Anti-platelet drugs

45
Q

What causes cerebral hemorrhage

A 
Hypertension (most common)
Head trauma
Congenital vascular abnormalities
Bleeding within infarction/tumor
Anticoagulants, illicit drugs
Cerebral amyloid angiopathy
46
Q

What happens in an arteriovenous malformation?

A

A direct connection forms between arteries and veins. This causes dilation of the vein due to increased pressure. There is a risk of rupture, hemorrhage.

47
Q

What is the management for a patient with a symptomatic berry aneurysm?

A

Identify bleeding with CT brain
Lumbar puncture to verify SAH (if normal CT)
Cerebral angiogram
Emergent clipping or endovascular coiling

MHD2 Block 2 - Neuro (26 decks)

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