CNS Response to Injury Flashcards

1
Q

Occurs when a sudden trauma causes damage to the brain

-Can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue

A

Traumatic Brain Injury (TBI)

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2
Q

When the brain slides forward and hits the frontal bone then backwards and hits the parietal bone

A

Coup-Contrecoup

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3
Q

Contrecoup contusions are more frequent than coup contusions in

A

Falls

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4
Q

Diffuse axonal injury can be seen histologically with

A

Beta Amyloid Precursor Protein (BAPP)

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5
Q

Associated with inflammation, gliosis & other pathological responses

A

TBI

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6
Q

The injury site is invaded by astrocytes, forming a

A

Glial Scar

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7
Q

A long-term problem of CNS injury is

A

Inflammation

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8
Q

Repeated sports-related head injuries results in concentrations of

A

Hyper p-tau protein (dark regions)

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9
Q

Hyper p-tau protein concentrations cause

A

Chronic Traumatic Encephalopahty (CTE)

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10
Q

Results in regional cerebral atrophy and can cause cavum septum pellucidum

A

CTE

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11
Q

We can see chronic neurodegeneration after a

A

TBI

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12
Q

A rapid blockage of a cerebral artery

A

Ischemic Stroke

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13
Q

Bursting of a vessel

A

Hemorrhagic stroke

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14
Q

Characterized by sudden numbness or weakness, especially on one side of the body

  • Sudden confusion or trouble speaking or understanding speech
  • Sudden trouble seeing in one or both eyes
A

Stroke

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15
Q

Both cause cell death due to lack of oxygen and production excytotoxins and free radicals

A

CNS stroke and Severe TBI

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16
Q

Excessive activation of neuronal glutamate receptors by a group of L-glutamate analogs results in

A

Neuronal Damage

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17
Q

Any chemical possessing unpaired electrons

-In biological system these are oxygen radicals

A

Free radicals

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18
Q

Causes loss of muscle and negative nitrogen balance, decreased gluconeogenesis, osteoporosis, increased hepatic lipogenesis, increased lipolysis in adipose tissue, decreased lipoprotein lipase activity in muscle and adipose tissue, cachexia

A

Chronic inflammation

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19
Q

Anemia of chronic disease, leukocytosis (high white blood cell counts), thrombocytosis (high platelet counts)

A

Hematopoetic changes in chronic inflammation

20
Q

What do we use to manage the inflammatory response of spinal cord injury?

A

Methylprednisolone, Erythropoetin, and Minocycline

21
Q

Causes tissue disruption and primary cells death

A

Spinal Cord Injury (SCI)

22
Q

Injured spinal cords show progressive

A

Tissue loss

23
Q

With an SCI, central hemorrhage necrosis develops over

24
Q

With an SCI, white matter blood flow falls by

A

50% within 3 hours

25
Metabolism is compromised with high lactic acid levels with an
SCI
26
Intracellular calcium activity >1µM activates proteases and phospholipases, breaking down proteins and lipids with an
SCI
27
This calcium then binds to mitochondria and produces
Free radicals
28
After injury, we begin to see neuronal apoptosis in the gray matter surrounding the injury. This peaks at
48 hours
29
We also see oligodendroglial apoptosis after injury in white matter tracts. This peaks
10-14 days after injury
30
We see breakdown of the blood brain barrier and rapid pro-inflammatory cytokine response (<1 h) with
SCI
31
Distal to the SCI lesion, we see
Wallerian degeneration
32
Severed spinal cord axons fail to
Regenerate
33
We get axonal degeneration and loss of myelin where?
Distal to an SCI injury
34
Disrupt axon extension in CNS injury
Inhibitory factors
35
We get a growth cone and axon growth-promotoing signals with
PNS injury
36
Can regenerate
PNS axons
37
Can induce central axons to regenerate
Sciatic nerve grafts
38
May be capable of regenerating given the appropriate environment
Central axons
39
Block regeneration
Glial scars
40
What are 4 exampls of inhibitory factors in the glial scar?
Myelin basic protein, Nogo A, MG, and OMgp
41
Inhibits growth of CNS axons
Nogo
42
Leads to long-distance regeneration and functional recovery in rats treated with anti-antibodies
Deactivation of Nogo A
43
What are three commonly used cell types to attempt to regenerate CNS axons after SCI?
OECs, Schwann cells, Neural Stem calls, and Embryonic stem cells
44
We can use human embryonic stem cells to derive
Oligodendrocyte precursor cells
45
We also can see axon emergence from grafts with human
Neuroprogenitor Cells (NPCs)
46
Can induce central axons to regenerate
Sciatic nerve grafts