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Neuroscience Week 6: Cerebrovascular disease Flashcards

1
Q

Overview

A
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2
Q

Objectives

A
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3
Q

Cerebrovascular diseases overview

A
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4
Q

Identify

A

15-20%

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5
Q

Identify

A
  • third most common
  • serious disabilities
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6
Q

Identify

A

ischemic necrosis (infarction) or hemorrhage

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7
Q

Cerebrovascular events (strokes) result from?

A
  • locally occlusive vascular disorders
  • reduction in systemic perfusion or oxygenation
  • hemorrhage
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8
Q

Describe cerebral perfusion

A
  • brain perfusion is heavily regulated
  • MAP doesnt change between 50 - 100 mmHg
  • also depends on concentration of CO2
  • when conc of PCO2 increases you have an increase in cerebral blood flow until 90mmhg
  • when O2 falls below 50mmhg there is an increase in cerebral blood flow
  • (tries to prevent hypoxia)
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9
Q

Strategies to treat acute cerebral edema

A

Therapeutic hyperventilation

when ↓ PCO2 there is vasoconstriction which ↓ cerebral blood flow → ↓intracranial pressure (ICP)

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10
Q

Therapeutic hyperventilation can be used to treat?

A
  • acute cerebral edema
  • when ↓ PCO2 there is vasoconstriction which ↓ cerebral blood flow → ↓intracranial pressure (ICP)
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11
Q

Global Cerebral Ischemia Causes

A

Caused by severe systemic hypotension (systolic blood pressure falls below 50 mmHg) secondary to cardiac arrest or shock

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12
Q

Global Cerebral Ischemia which cells are more susceptible

A
  • Neurons are more susceptible than glial cells
  • The pyramidal neurons in the hippocampus and neocortex are particularly vulnerable
  • as are the Purkinje cells in the cerebellum
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13
Q

Describe Severe Global Cerebral Ischemia

A
  • widespread neuronal death occurs
  • survivors will have severe neurological deficits (vegetative state or brain death)
  • All voluntary and brainstem reflex functions are absent requiring mechanical ventilation
  • the brain undergoes autolysis
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14
Q

Global Cerebral Ischemia Overview

A
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15
Q

Global Cerebral Ischemia Gross Morphology

A

Swollen brain with wide gyri and narrowed sulci

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16
Q

Global Cerebral Ischemia Histology: Early changes (12-24 hours)

3 listed

A

Early changes (12-24 hours)

  • cystoplasmic eosinophilia (red neurons)
  • nuclear pyknosis and fragmentation
  • Glial cell damage also occurs and neutrophil infiltration
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17
Q

Global Cerebral Ischemia Histology: Subacute changes (24hrs-2 weeks)

A
  • Necrosis
  • macrophage infiltration
  • vascular proliferation
  • reactive gliosis
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18
Q

Global Cerebral Ischemia Histology: Repair (2 weeks)

A

removal of necrotic tissue and gliosis

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19
Q

Identify

A

Global Cerebral Ischemia

infiltration of cerebral infarction by neutrophils begins at the edges of the lesion where the vascular supply is intact

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20
Q

Identify

A

Global Cerebral Ischemia

By day 10, an area of infarction shows the presence of macrophages and surrounding reactive gliosis

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21
Q

Identify

A

Global Cerebral Ischemia

Old intracortical infarcts are seen as areas of tissue loss and residual gliosis

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22
Q

Identify

A

Global Cerebral Ischemia

A. infiltration of cerebral infarction by neutrophils begins at the edges of the lesion where the vascular supply is intact

B. By day 10, an area of infarction shows the presence of macrophages and surrounding reactive gliosis

C. Old intracortical infarcts are seen as areas of tissue loss and residual gliosis

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23
Q

Identify

A
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24
Q

Global Cerebral Ischemia Watershed Infarcts

A
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25
Q

Identify

A

Watershed infarction at MCA/PCA territory

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26
Q

Identify

A

Watershed infarction at ACA/MCA territory

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27
Q

Embolic Infarctions Common Causes

3 listed

A
  • Cardiac mural thrombi are frequent cause of emboli (e.g. in patients with atrial fibrilation, myocardial infarction or valvular disease).
  • Thromboemboli can also originate in carotid atheromatous plaques
  • Venous emboli can cross into the arterial circulation via a patent foramen ovalae (deep venous thrombosis of legs or fat embolism)
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28
Q

Embolic Infarctions commonly affect which vessel

A

Commonly affect MCA

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29
Q

Thrombotic Occlusions Common Causes

2 listed

A
  • Superimposed on atherosclerotic plaques in carotid bifurcation, MCA origin, and ends of the Basilar artery
  • can also be caused by hypertension-induced thrombotic occlusions of small penetrating arteries (lacunar infarcts)
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30
Q

Acute non-hemorrhagic infarcts can?

A

Evolve into hemorrhagic infarcts

especially when there is reperfusion of ischemic tissue (either through collaterals or after emboli have dissolved)

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31
Q

Focal Cerebral Ischemia Examples

3 listed

A
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32
Q

Identify

A

Cerebral infarction

A. Section of the brain showing a large, discolored, focally hemorrhagic region in the left middle cerebral artery distribution (hemorrhagic, or red, infarction)

B. An infarct with punctate hemorrhages, consistent with ischemia-reperfusion injury, is present in the temporal lobe

C. Old cystic infarct shows destruction of cortex and surrounding gliosis

33
Q
A

Cerebral infarction

A. Section of the brain showing a large, discolored, focally hemorrhagic region in the left middle cerebral artery distribution (hemorrhagic, or red, infarction)

34
Q

Identify

A

Cerebral infarction

B. An infarct with punctate hemorrhages, consistent with ischemia-reperfusion injury, is present in the temporal lobe

35
Q

Identify

A

Cerebral infarction

C. Old cystic infarct shows destruction of cortex and surrounding gliosis

36
Q

Macroscopic classification of Non-hemorrhagic infarcts

A
  1. Acute
  2. Subacute

&

  1. Remote
37
Q

Describe features and classification

A
  • Acute
  • Initially appears pale and edematous soft to palpation (first 48 hours)
  • Edema can cause death by subsequent herniation
38
Q

Describe features and classification

A
  • Subacute
  • Becomes gelatinous with more obvious delineation from normal tissue (2-10 days)
39
Q

Describe features and classification

A
  • Remote
  • Tissue liquefies, leaves a fluid-filled cavity lined by dark tissue (10 days - beyond)
40
Q

Describe the features and stage of this infarct

A

Acute stage

  • red neurons
  • Edema (Vacuolation of neuropil)
  • Neutrophils present at about 24 hours, then disappear mostly by 48 hours)
41
Q

Describe the features and stage of this infarct

A

Subacute

  • Macrophages appear and predominate
  • Tissue defect is obvious
  • Astrocytes proliferate at the edge and become reactive (1 week)
42
Q

Describe the features and stage of this infarct

A

Remote

  • Cavity will contain glial fibers, new capillaries and connective tissue fibers
43
Q

Primary Brain Parenchymal Hemorrhage age of onset

A

Most common in mid to late adult life (peak at 60 years of age)

44
Q

Primary Brain Parenchymal Hemorrhage Common etiology

A

Most commonly caused by hypertension

45
Q

Primary Brain Parenchymal Hemorrhage location

A
  • 70-80% of hypertensive hemorrhages occur in the lenticulostriate and thalamostriate arteries which supply the basal ganglia, internal capsule and thalamus
  • 5-10% of hemorrhages arise in the lobar white matter of the cerebral hemispheres
46
Q

Primary Brain Parenchymal Hemorrhage Infratentorial sites

A
  • ~15-20% of all cases
  • include the basal pons and cerebellar white matter
47
Q

Primary Brain Parenchymal Hemorrhage Infratentorial sites Prognosis

A

Hemorrhages into the pons are nearly always fatal, while hemorrhages into the cerebellum can cause rapid decreases in pressure in the posterior fossa and are a neurosurgical emergency but are frequently survivable

48
Q

Primary Brain Parenchymal Hemorrhage Hypertensive Hemorrhages

A
  • hypertensive hemorrhages are the result of hypertension-induced degenerative changes in arterial or arteriolar walls probably combined with increased perfusion pressure
  • The role of (charcot-Bouchard) microaneurysms has been difficult to substantiate in most cases
49
Q

Primary Brain Parenchymal Hemorrhage Pathology

A
  • Hypertensive hemorrhages typically give rise to large hematomas
  • Ventricular extension of the hematoma is common in fatal cases of hemorrhage in the basal ganglia, thalamus or pons
  • Mass effect occurs due to both the hematoma and surrounding edema
  • This expansile effect often is severe enough to cause herniation
  • Resolution of a survivable hemorrhage may leave a surprisingly small tissue defect
50
Q

Hemorrhages appearance

51
Q

Cerebral Amyloid Angiopathy Description

A
  • β-amyloid can also deposit around blood vessels
  • most commonly the leptomeninges (this is not always a feature of Alzheimer’s Disease)
  • Can be a source of intraparenchymal hemorrhage
52
Q

Lobar Hemorrhages

53
Q

Subarachnoid Hemorrhage Location & cause

A
  • Most common cause is a rupture of saccular aneurysms (circle of Willis and proximal MCA in ~90%)
  • they may be in multiple (in up to 15-20% of cases)
  • Other causes can be vascular malformation
  • and
  • Trauma
54
Q

Subarachnoid Hemorrhage Clinical Presentation

A
  • Occur at time of increase in intracranial pressure (e.g. defacation or orgasm)
  • Thunderclap headache followed by loss of consciousness
55
Q

Subarachnoid Hemorrhage Etiology

A

Saccular aneurysms are due to weakening and thinning of the arterial wall with aneurysmal dilation

Lack of muscular wall and intima elastic lamina (sac is lined by thickened hyalinized intima)

56
Q

Subarachnoid Hemorrhage Risk considerations

A

Increased risk in patients with polycystic kidney disease and extracellular denetic disorders (Ehler-Danlos)

57
Q

Subarachnoid Hemorrhage Pathology

A
  • The size on an aneurysm is important (~0.5-1cm diameter is most likely to rupture)
  • Rebleeding is common if the aneurysm is not surgically clipped or occluded
  • Intracerebral hemorrhages result from rupture of an aneurysm directly into brain parenchyma (and/or ventricles)
58
Q

Subarachnoid Hemorrhage Complications

A
  • Secondary infarction which usually is attributed to vasospasm
  • Arachnoid fibrosis which his due to the organization of hemorrhage in the meninges in patients who survive
  • Later sequela of arachnoidal fibrosis can include hydrocephalus due to interference with the flow of CSF
59
Q

Subarachnoid Hemorrhage Prognosis

A

High mortality (25-30% die within 24 hours, 50% by one month, and 60% by 1 year)

For those alive after 6 months approximately 70% have no major neurological deficits, 20% have partial neurological deficits and 10% have a permanent disability

60
Q

Identify

61
Q

Identify

62
Q

Vascular Malformations Most common form

A

Arteriovenous malformation (AVM) is the most common type and more dangerous

63
Q

AVM AKA

A

Arteriovenous malformation

64
Q

Arteriovenous malformations (AVM) Description

A

are complex direct shunts from the arterial to the venous system with intervening gliotic brain parenchyma

65
Q

Arteriovenous malformations (AVM) Clinical presentation

A

may present with seizures (from local ischemic damage to “vascular steal” from cerebral cortex in the area of the shunt prior to developing hemorrhage

66
Q

Arteriovenous malformations (AVM) vessel involvement

A

AVMs typicallyt involve both the arachnoidal and intraparenchymal vessels

They have high flow and arterial pressures that predispose them to rupture and hemorrhage which may be intraparenchymal, subarachnoid or both

67
Q

Arteriovenous malformations (AVM) Prognosis

A

These hemorrhages are often massive and frequently fatal (more hypertensive/amyloid etiologies in a young person)

68
Q

Hypertensive Cerebrovascular Disease description

A

Hypertension causes hyaline sclerosis of deep penetrating arteries and arterioles that supply basal ganglia, hemispheric white matter and brain stem

69
Q

Charcot-Bouchard microaneurysms can form in?

A

Small vessels

70
Q

Hypertensive Cerebrovascular Disease can cause

4 listed

A
  • intracerebral hemorrhage
  • Lacunar infarcts
  • Rupture of a small-caliber penetrating vessel
  • Acute hypertensive encephalopathy
71
Q

Lacunar infarcts

72
Q

Lacunar infarcts description and etiology

A
  • small cavity infarcts in basal ganglia and thalamus, internal capsulel, deep white matter and pons
  • Caused by occlusion of small penetrating branches (most commonly the lenticulostriate vessels
73
Q

Rupture of a small-caliber penetrating vessel

A

small hemorrhage that leaves a slit-like cavity (slit hemorrhage)

74
Q

Acute hypertensive encephalopathy etiology and common features

A
  • caused by diastolic BP increases >130 mmHg
  • Characterized by increased intracranial pressure and global cerebral dysfunction
  • Brain edema (herniation in some cases)
  • Petechia and fibrinoid necrosis of arterioles in gray and white matter
75
Q

Identify

76
Q

Vasculitis etiology

A
  • Caused by inflammatory processes involving blood vessels
  • Infectious arteritis (aspergillosis, herpes zoster, cytomegalovirus) in immunosuppressed patients
77
Q

Polyarteritis Nodosa and Giant cell (temporal) arteritis

A
  • Common forms of Vasculitis
  • which are more frequent in older people and women and is associated with polymyalgia rheumatica
78
Q

Vasculitis Pathology and clinical presentation

A
  • primary angiitis of the CNS affecting multiple parenchymal and subarachnoid vessels
  • characterized by chronic inflammation, multinucleate giant cells and vessel wall destruction
  • Present as diffuse encephalopathy with cognitive dysfunction
79
Q

Identify

A
  • Giant Cell (temporal) Arteritis
  • Disruptions of the elastic lamina with inflammation and giant cells

FMS (34 decks)

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