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Neuroscience: Exam 3 > Lecture 8: Neural Response to Ischemic Injury and Stroke > Flashcards

Lecture 8: Neural Response to Ischemic Injury and Stroke Flashcards

1
Q

What are modifiable risk factors of stroke?

A
  • high BP
  • High Body mass index
  • high fasting glucose
  • poor diet
  • high LDL
  • Kidney dyfunction
  • air pollution
  • alcohol use
  • smoking
  • low physical activity
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2
Q

What are Unmodifiable risk factors of stroke?

A
  • Age
  • Gender
  • Genetics
  • Head/ Neck Injuries
  • Pregnancy
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3
Q

What is a stroke?

A
  • Sudden loss of blood supply to brain tissue as a result of either a blocked or burst blood vessel
  • Loss of oxygen and nutrients leads to neural cell death (infarction)
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4
Q

What are the two types of strokes?

A
  • Hemorrhagic stroke (15%)
  • Ischemic stroke (85%)
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5
Q

What are the two types of Hemorrhagic strokes?

A
  • Intracerebral hemorrhage: in brain tissue
  • Subarachnoid hemorrhage: btw pia layer and arachnoid layer-> bleeding in the space that surrounds the brain-> MOST DEADLY
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6
Q

What are the two types of ischemic stroke?

A
  • Thrombotic strokes: caused by a blood clot that develops in the blood vessels inside the brain.
  • Embolic strokes: Ouside of CNS-> when a blood clot or debris (embolus) travels from one part of the body and lodges in a narrower brain artery
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7
Q

Where do 65% of strokes occur in?

A

territory of the middle cerebral artery

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8
Q

Where do 15-25% of strokes occur? 10%?

A

15-25% occur in the Posterior circulation

  • Occlusion supplying the brainstem often leads to death
  • Otherwise effects are not as severe
  • Occlusion supplying the brainstem (basilar artery) often leads to death

10% of strokes occur in watershed areas

  • out towards the capillary bed and towards the system so it can have a global effect
  • in watershed areas (near capillary beds)
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9
Q

After MCAO, regions which sustain damage include:

A
  • Dorsolateral Striatum (usually damaged)
  • Neocortex (usually damaged)
  • Hippocampus (caused by larger strokes)
  • Thalamus (secondary injury)
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10
Q

Is the middle cerebral artery or posterior circulation stroke worse? explain?

A

Posterior circulation stroke because there no no other way to get blood around the brain since all the arteries come together at the basilar artery -> EITHER MAJOR EFFECT OF NO EFFECT

Middle cerebral has another side to supply the brain

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11
Q

External carotid supplies what? which sends collaterals to the brain via what? (2)

A
  • External Carotid supplies facial artery which sends collaterals to the brain via the internal carotid
  • External Carotid supplies superficial artery which also sends collaterals to the brain via the internal carotid

Bold: how we connect the two

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12
Q

External to vertebral artery connects through what?

A

External Carotid supplies the occipital artery which sends collaterals into the vertebral artery

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13
Q

External to internal
1. external->
2. external->

A
  1. Facial
  2. superficial
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14
Q

External to Vertebral

  • External->
A

occipital

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15
Q

what are the Leptomeningeal branches?

A

Watershed areas (Anastasomes)

  • Anterior cerebral artery
  • middle cerebral artery
  • posterior cerebral artery
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16
Q

List all the collateral blood flow (5)

A
  1. External -> facial
  2. External -> superficial
  3. External -> occipital
  4. Circle of Willis
  5. Leptomeningeal-> anterior, middle, posterior
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17
Q

What is unique about the cicle of willis?

A

If you get damage on your right side, flow on the left may compensate for losses on the right side

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18
Q

What is the importance of collateral flow in Recannulation?

A

When you have high collateral flow, the infract will not be seen because blood will reach there

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19
Q

What are the regions that are damage after MCAO?

A
  • NeoCortex , Dorsal-lateral striatum, corpus callsum, Hippocampus
  • Thalamus-> considered a 2nd injury
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20
Q

The types and degrees of disability that follow a stroke depend upon what?

A

area of the brain is damage and how much damage is there

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21
Q

What are the five types of disabilities caused by stroke?

A
  1. Paralysis or problems controlling movement
  2. Sensory disturbances including pain
  3. Problems using or understanding language
  4. Problems with thinking and memory
  5. Emotional disturbances
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22
Q

What are the sensory distrubances after stroke?

A
  • lose the ability to feel touch, pain, temperature, or position
  • neuropathic pain-> nothing will stop it completely
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23
Q

What are problems using or understanding language after stroke?

A
  • One-fourth of all stroke survivors experience language impairments
  • Broca’s area, causes expressive aphasia (can understand words but cannot respond to them)
  • Wernicke’s area, results in receptive aphasia (cannot understand but can talk)
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24
Q

What are the problems with thinking and memory after stroke?

A

shortened attention spans or may experience deficits in short- term memory

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25
Q

What are the emotional distrubances after stroke?

A
  • fear, anxiety, frustration, anger, sadness, and a sense of grief -> depends on what area you damage
  • clinical depression is common-> not sure if it is damage or just dealing with the stroke
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26
Q

What is the core of a stroke?

A
  • the region that lost direct vascularization
  • Cells within this region usually die within minutes and create an infarct
  • Place that loses vascularization
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27
Q

What is the area surrounding the core?

A

Penumbra

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28
Q

What is happening in the penumbra from a stroke?

A
  • Although this area did not directly lose blood flow, the damage caused at the core leads to inflammation and apoptosis.
  • Compensatory reactions such as acidosis decrease protein synthesis, and selective gene expression within this region intensify inflammation and can eventually lead to cell death if left untreated.
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29
Q

What happens in the immediate phase?

A
  • Vascular thrombosis
  • Platelet embolization
  • BBB permeability
  • Metabolic stress -> Increase lactate, decrease ATP
  • Ionic perturbations (Ca++, Na+, K+)
  • Anoxic depolarization (cortical spreading depression)-> no O2 so trouble firing APs
  • Cytokine release
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30
Q

What happens in the acute phase?

A
  • Selective neuronal damage (necrosis)
  • Inflammation (PMNLs, Macrophages, lymphocytes, microglia)
  • Vascular reactivity abnormalities
  • glial swelling
  • secondary axotomy

Phase II

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31
Q

What happens in the subacute phase?

A
  • Apoptosis
  • Protein Aggregation
  • Cell signaling perturbations
  • Gene expression (HSP, Growth factors)
  • Axonal Damage (permanent, transient, delayed)
  • Axonal transport abnormalities
  • Wallerian degeneration

phase III

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32
Q

What happens in the ultimate outcome

A
  • Infaract formation
  • progressive tissue loss (atrophy)
  • Functional deficits (behavioral and electrophysiological)

Phase 4

33
Q

What is happens in the brain after a stroke?

34
Q

What does neuropatholgy affect?

A

all cell populations in the CNS

35
Q

What happens to neurons, astrocytes, and oligodendrocytes during neuropathy?

A
  • Necrotic & Apoptotic cell death
  • Cellular inclusions
  • Vaculoation of neurons/neuropil Binucleated
  • Neurofibrillary tangles
  • Neuronal storage disorder
  • Edema (axon, astrocyte processes)
36
Q

What happens to glial cells during neuropathology?

A
  • Nuclear hypertrophy
  • Scar forming
37
Q

What is the glial response to brain injury?

A

oligodendrocytes. astrocytes and microglia respond

38
Q

How do oligodendrocytes respond to brain injury?

A

like neurons-> dying

39
Q

What are astrocytes and how do they respond to brain injury?

A
  • Neuronal support cells
  • React to injury becoming enlarged and expressing increased glial fibrillary acidic protein
  • Wall off injured area-> so dying neural cells cannot affect the area around

will recycle it back into the tissues

40
Q

What are microglia and hoe do they respond to brain injury?

A
  • Macrophages of the brain
  • React to injury becoming phagocytic and releasing inflammatory cytokines
  • Responsible for delayed neuronal death
41
Q
  • When do you want microglia present?
  • When do you not want them present?
A
  • You want them early on at the site of damage to get rid of all the debris for repair
  • You do not want them 48-72 hours after when perpherial immune cells come in
42
Q

What are two ways neurons die after stroke?

A
  • Necrosis-> no going back and happen quickly
  • Apoptosis ->affects the penumbra layer
43
Q

What is the difference of necrosis and apoptosis?

44
Q

What are two ways of visualizing dying neurons?

A

TTC and Fluorojade

45
Q

How does TTC work?

A

Vital dye

  • Dye used to detect vitality of tissue shortly after stroke/trauma-> Good for early detection
  • If cells are alive they take up the red dye and white areas are dead cells
46
Q

How does Fluorojade work? ⭐️

A

good for later on

  • Basic dye that is attracted to acidified cells (dt to lactate acid+glutamate)
  • More sensitive than most other histochemical methods
  • Easy to use and can see individual populations unlike TTC
  • Fluorescent green shows dead cells
47
Q

How does astrocytes react to injury?

A
  • React to injury becoming hypertrophic (enlarged) and expressing increased glial fibrillary acidic protein (GFAP)
  • Wall off injured area
48
Q

How are astrocytes after a stroke with and without DTG?

A
  • Without: see the boarding of astrocytes
  • With: do not see them walling off, less damage
49
Q

What happens to oligodendroglials after stroke? What can we use to help?

A
  • oligo lose myelin basic protein
  • Can use HUCBC (cord blood cells) to lessen the damage
50
Q

What happens to oligodendroglials after stroke? What can we use to help?

A
  • oligo lose myelin basic protein and the production of neuronal myelin sheath. Decreased AP propagation
  • Can use HUCBC (cord blood cells) to lessen the damage
51
Q

How does the microglial respond to stroke?

A

Increase after stroke

  • React to injury becoming phagocytic and releasing inflammatory cytokines
  • Responsible for delayed neuronal death
52
Q

What is the unifying pathophysiolic mechanisms of CNS injury

53
Q

What is inflammation?

A

a protective response occurring in the vascularized connective tissue in response to an insult

54
Q

What does inflammation response to?

A
  • Bacteria
  • Virus
  • Tissue Injury
  • Pattern Recognition Receptor on antigen presenting cells respond to PAMPs (bacteria) or DAMPs (tissue damage) that binds to toll like receptors
55
Q

What does inflammation remove and what is the result?

A
  • Removes noxious agents, thereby limiting their detrimental effects
  • Becomes dysregulated with age
  • uncontrolled inflammation may be harmful and may underlie the pathogenesis of many acute and chronic diseases
56
Q

Explain the beginning pathway of inflammation

A

In stroke patients, inflammatory cascades are triggered by the release of endogenous molecules by damaged tissue and necrotic cells. These endogenous molecules will bind to pattern recognition receptors (i.e. DAMPs) which illicit the NFkB pathway.

57
Q

Why is inflammation a double edged sword?

A

During instances of neuronal injury, microgliosis can have two effects: tissue repair and recovery OR chronic disease progression.

  • Tissue repair and recovery is mediated by timely and well-regulated inflammation which can remove noxious agents and limit their detrimental effects.
  • Uncontrolled inflammation, however, may be harmful and an underlie the pathogenesis of many acute and chronic diseases
58
Q

look at slide 28

59
Q

What is the function of neurotrophic factors?

A

secrete proteins that modulate neuronal growth, differentiation, repair, and survival; some have additional functions, including roles in Neurotransmission and in the synaptic reorganization involved in learning and memory

60
Q

What are the different neurotrophins and their correlating receptors?

A
  • TrkA receptor: NGF
  • TrkB receptro: BDNF, NT-4/5, NT-3
  • TrkC receptor: NT3
  • p75 receptor: all of them above
61
Q

Explain the signal cascade for trk receptor

62
Q

Explain the signal cascade for p75 receptor

63
Q

What are the other neurotrophic factor families

64
Q

What does BDNF do?

A

central role in neuronal survive because have repairative affects in brain

65
Q

Explain the structural organization of NF-KB, IKB, IKK

66
Q

Explain the activation of the canonical NF-KB pathway

A

Activation of the canonical NF-kB pathway culminates in the translocation of NF-kB dimers (p65/cRel + p50) into the cell nucleus. This activates gene transcription of pro-inflammatory mediators.

67
Q

Explain the activation of the alternative NF-B pathway

68
Q

What happens when there is a lack of p50?

A

increase vulnerability to neurotoxic insult

69
Q

What are questions about research models?

70
Q

What is 1,3-Di-O-Tolylfuanidine (DTG)? Function?

A

Selective Sigma 1 and Sigma 2 receptor ligands

Neuroprotective

  • Inhibits ischemia-induced cell death
  • Regulates Ca2+ homeostasis and membrane excitability
  • Upregulates neuroprotective genes

Anti-inflammatory

  • Inhibits microglial inflammatory responses
71
Q

What does DTG do?

A

Decreases Neurodegeneration as Indicated by Fluoro

72
Q

How was DTG short term and long term?

A

Very good short term but long term results (5 weeks) there was no improvement of behavior and tissue

73
Q

What is important about therapeutic targets for strokes

A

need to focus on more than one effect

74
Q

What is the preclinical STAIR Criteria to enhance translation of stroke therapies?

75
Q
  1. A 67-year-old man is rushed to the ED following sudden numbness of his face and difficulty seeing out of his right eye. The patient is immediately placed on blood thinners after MRI confirms the presence of a blood clot which led to an ischemic stroke. In which of the following arteries is the blood clot most likely located?
    A. Anterior cerebral artery (ACA)
    B. Middle cerebral artery (MCA)
    C. Posterior cerebral artery (PCA)
    D. Basilar artery
A

B. Middle cerebral artery (MCA)

76
Q
  1. Metabolic stress due to decreased ATP production and increased lactate production are characteristic of what phase following cerebral ischemia?
    A. Immediate
    B. Acute
    C. Subacute
    D. Outcome
A

A. Immediate

77
Q
  1. Scientists at the Morsani College of Medicine are studying oligodendrocyte responses to ischemic stroke using fluorescent dyes and microscopy. Which of the following are the scientists most likely to observe under the microscope?
    A. Widespread acidification due to necrotic death
    B. Hypertrophy and increased GFAP production
    C. Chronic release of inflammatory cytokines
    D. Depleted production of myelin basic protein
A

D. Depleted production of myelin basic protein

78
Q
  1. Following a stroke, inflammation is considered a “double-edged sword” that can lead to recovery or further disease progression. Which of the following accurately describes the effect of the alternative NF-kB pathway as it relates to cerebral ischemia?
    A. ↑ pro-inflammatory mediators via nuclear p50 translocation
    B. ↑ pro-inflammatory mediators via nuclear p52 translocation
    C. ↓ pro-inflammatory mediators via nuclear p50 translocation
    D. ↓ pro-inflammatory mediators via nuclear p52 translocation
A

B. ↑ pro-inflammatory mediators via nuclear p52 translocation

79
Q
  1. All of the following neurotrophic factors bind to TrkB receptors EXCEPT:
    A. NGF
    B. BDNF
    C. NT-4/5
    D. NT-3

Neuroscience: Exam 3 (9 decks)

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