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NEURO 411 > Cerebrovascular function - Ian Winship > Flashcards

Cerebrovascular function - Ian Winship Flashcards

1
Q

What does the circle of willis have?

A

Collateral vasculature

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2
Q

Do capillaries have smooth mm.?

A

No; but can have pericytes

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3
Q

What is an ischemic stroke

A

85% of strokes due to blockage of a cerebral vessel

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4
Q

What are the two forms of ischemic stroke?

A

Thrombic –> area of vessel irritated, thus forming clots; thromboembolic –> clot travels from somewhere else

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5
Q

What is an hemorrhagic stroke?

A

Rupture of blood vessel

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6
Q

Is mortality greater for H. stroke?

A

Yes, 40-50% early mortality in subarachnoid hem.

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7
Q

What is subarachnoid hem caused by?

A

Raised intracranial pressure, vasospasm (constriction of blood vessels for days, thus also causing I.stroke)

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8
Q

Describe intracerebral hemorrhage stroke?

A

Vessels ruptures leaking blood into parenchyma, thus causing mechanical disruption and blood toxicity; more common with hypertension diabetes due to stiff BV

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9
Q

What type of arteries are commonly affected in intracerebral hem?

A

lenticolostriate arteries as they are connected to high-pressure BV

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10
Q

What is the stroke core and penumbra?

A

Stroke core: tissue dies immediately where vessel ruptures; penumbra is surrounding and doesn’t die immediately due to BV collaterals

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11
Q

How does stroke initiate ischemic cascade?

A

no blood = decrease ATP –> acidosis (anaerobic compensation) –> failure of Na/K pumps –> mem. depolarization –> glutamate excitotoxicity —> increase Ca+ leading to necrotic + apoptotic cell death

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12
Q

What does capsase 3 mean?

A

Apoptosis (programmed cell death)

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13
Q

What does LC3 and Beclin 1 mean?

A

Repair/recycling processes are impaired (autophagy)

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14
Q

What does pycnotic cells mean?

A

Necrosis at stroke core (rapidly depolarizing and lysing cells)

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15
Q

What are pannexins? (panx)

A

Panx are large pore channels that indescrimnantly lets things in (positive ions come in and stay in)

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16
Q

What does blocking panx do?

A

Stops anoxic depolarization; however, injury comes within minutes so its hard to block panx at right time

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17
Q

Describe the extrinsic pathway in apoptosis?

A

Receptor activation leads to activation of caspase 8, thus activating caspase 3

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18
Q

Describe the intrinsic pathway in apoptosis?

A

Mitochondrial stress opens MPTP, releases Cytochrome C, activates caspase 9 and then activates caspase 3

19
Q

What is the apoptosis induced factor (AIF)?

A

Regulates cascade-independent pathway in apoptosis (no caspase 3)

20
Q

Where does apoptosis occur?

A

Outside of stroke core, in pneumbra

21
Q

What is diaschisis?

A

Area of NS connected with injured area shows decreased metabolism due to loss of reciprocal connections that maintain neural activity

22
Q

Does diaschisis show atrophy?

A

Yes

23
Q

Describe focal diaschisis at rest?

A

Decreased energy metabolism

24
Q

Describe focal diaschisis while functioning?

A

Abnormalities in metabolism and neuronal activity

25
Q

Describe connectional diaschisis?

A

Selective change in coupling between two notes of a defined network, involves areas distant from lesion

26
Q

Describe connectional diaschisis?

A

Change in structural and functional connective, including disconnection/reorganization of subgraphs (includes all connections in brain and is mostly theoretical )

27
Q

What is GAP-43?

A

Growth associated protein found in axonal cores that helps with spinal plasticity after stroke

28
Q

How does the corticospinal tract (CST) regulate stroke outcome?

A

increased integrity increases motor performances/recovery

29
Q

Has amyloid been found in stroke hemispheres and is it important?

A

Yes, can cause secondary Neurodegeneration; hasn’t been studied much, thus no evidence of amyloid as a key mediator

30
Q

What causes delayed schema in Subarachnoid Hem. stroke?

A

Vasospams; overall cause cognitive impairment

31
Q

What commonly causes global schema?

A

Heart attacks

32
Q

Which area of the brain is particularly susceptible to global ischemia?

A

CA1 (important in learning/memory)

33
Q

What are the characteristics of chronic hypo perfusion?

A

Researchers cut of Common carotid, thus only leaving anterior circulation;

Overall, reduced blood flow, reduced cognition and reduced in hippocampal volume. However, no motor symptoms

34
Q

What does hypo perfusion do mechanism wise?

A

Oxidative stress; hypoxia; inflammation

Importantly, it causes endothelial dysfunction which impairs auto regulation. There is also BBB breakdown which leads to influx of more damaging factors.

35
Q

What does the BBB breakdown lead to?

A
  • accumulation of toxic factors, like thrombin
  • Faulty transport thus decrease in LRP1 (amyloid effluxer), increase in RAGE (amyloid influxer)
  • RBC lysing, microbleeds, Fe+
  • Inflammation etc
36
Q

what is the neurovascular unit?

A

Various cells regulating blood flow; pericyte, endothelium, basement membrane, microglia, astrocyte, oligodendrocyte, neuron

37
Q

What are the mechanisms of vascular dementia?

A
  • Microbleed/microinfarcts
  • hypoperfusion
  • small vessel ATS, arteriosclerosis, deposit of fat in vessel –> all narrow BVs
  • ALL CASES LEAD TO NARROW BVs and HYPOERFUSION
38
Q

What are the types of vascular dementia?

A
  • Multi infaract (most common) step wise progression
  • Strategeic (focal): large vessel occlusion; never return to normal but can be slightly improved
  • White matter hyperintensity (atrophy based progression - steadier)
39
Q

What is the vascular hypotehsis in AD

A

Interaction bewteen A beta and vascualr risk factrs lead to impaired processing and AD pathology

40
Q

Is cerebrovascular function impaired in AD?

A

Yes

APOE4 has greater risk

41
Q

What is cerebral amyloid angiopathy?

A

Deposition of amyloid in** blood vessels** rather than brain; key contributor to cog. decline; causes hypoperfusion, white matter intesntiy,** perivascular space**; inflammation etc

42
Q

Describe the ischemic and hemorrhagic pathway in CAA:

A
  • Ischemia: Desposition of amyloid in BV-> impaired vasodilation (reactivity) and activity in brain -> microinfarcts, etc
  • Hem. : loss of **vascular integrity **–> rupture —> iron accumulation / symptomic hemorrhage (intracerebral hemorrhage)
43
Q

Can CAA patients increase Blood flow?

A

No; not able to increase blood flow in resposne to specific challenge

44
Q

Is cerebrovascular reactivity impaired in CAA?

A

Yes, so are AD and MCI; however, CAA more impacted than AD and MCI

NEURO 411 (12 decks)

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