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Brain and Behaviour > Injury and Repair of the Nervous system > Flashcards

Injury and Repair of the Nervous system Flashcards

1
Q

what happens after nerve injury

A
  • After revascularixation a composite tissue allograft is viable but it is not functional
  • The axons of the recipient have to regrow and replace the axons of the donor to reinnervate the muscles and the sensory end organs within the graft
  • The donor nerves severe as temporary scaffold for the axons to grow into
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2
Q

describe what happens with axonal damaged

A
  • initially the damage is localised and then it may spread to the synaptic boutons and towards the cell body as parts of the nerve is degenerated
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3
Q

what does anterograde degeneration mean

A

this involves the distal parts of the axon and occurs rapidly
- segment of the axon swell and break apart over 2-3 days

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4
Q

what does retrograde degeneration mean

A
  • involves changes to the proximal part of the axon from the site of damage to the soma over 2-3 days
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5
Q

what are the ways in which nerve segregation spreads

A

retorgrade degeneration

anterograde degeneration

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6
Q

what are the challenges of nerve repair

A
  • Nerve repair is not always successful
  • Nerve damage may spread
  • The success of repair depends on the severity of the injury (primary and secondary)
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7
Q

when is repair successful and when is it not successful

A
  • Repair may happen when damage is not localised but attempts might not be successful
  • Repair always happens when damage is localised
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8
Q

what does the success of nerve repair depend on

A
  • Severity of initial injury
  • Location of injury
  • the extent of Secondary damage
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9
Q

what is the spread of injury due to

A

trans neuronal degeneration

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10
Q

what do severed nerves do

A

Leave a lot of debris

Stop transmission

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11
Q

what is a primary injury

A

where nerve was cut but this is
never localised and it spreads (causing secondary
damage) by:

Anterograde degeneration/ Wallerian degeneration

Retrograde degeneration/ axonal die-back

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12
Q

what is primary damaged

A
  • what has been damaged

- how much has been damaged

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13
Q

what are the types of nerve injury

A

neurapraxia - mild
axonotemesis - moderate
neurotmetsis- severe

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14
Q

describe neurapraxia

A
  • this is loss of motor and sensory function due to blockage of nerve conduction
  • 1st degree damage
  • myelin is not in tact
  • it is reversible
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15
Q

describe Axonotmesis

A
  • a disruption of axons, resulting from severe crush or contusion
  • 2nd degree damage
  • myelin is not intact
  • axon is not intact
  • there is wallerain degeneration
  • it is reversible
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16
Q

describe Neurotmesis

A
  • Both the axons and nerve sheath are damaged
  • 3rd degree
  • myelin is not intact
  • axon is not intact
  • epineurium is not intact
  • there is wallerain degeneration
  • it is irreversible
17
Q

what happens when there is axon damage

A
  • Burst of action potentials stimulate the dorsal root ganglion of axon
  • This disrupts the retrograde transport flow of trophic support
  • Causes neurotrophic factors from innervated cells to be released and taken up by nerve terminals
  • Injury signals taken up by the cell body and cause:
  • Cells in dorsal root ganglion change phenotype from a transition
    state to a growth state by upregulating axonal growth proteins
18
Q

what do the neurotrophic factors do

A
  • released by innervated cells
  • taken up by the nerve terminals
  • transported retrogradely to the neuronal cell body to promote neuronal growth and survival
19
Q

what are the examples of neurotrophic factors

A
  • NGF: Nerve Growth Factor
  • BDNF: Brain-Derived Neurotrophic Factor
  • GDNF: Glial cell-Derived Neurotrophic Factor
20
Q

describe what happens with axon damage when there is severe damage

A

SEVERE injuries:

Wallerian degeneration may have to occur completely before
regeneration can start. This often leads to complete loss of
connection to spinal cord, in which regeneration cannot occur.

21
Q

how do cells conduct nerve regeneration

A
  • they are important for the process of repair
  • they divide and make a new portion of axons to be made
  • need more Schwann cells to do the myelination
  • also secrete neurotrophic factors to guide the axons
22
Q

what are the obstacles to successful regernation

A

Prolonged axotomy (severing) reduces
the number of neurons and axons that
can regenerate.

After 1 month: Schwann cells
down-regulate regeneration associated
factors.

Prolonged denervation causes muscle
atrophy and fibrosis.

23
Q

The proximal and distal part…

A

proximal part and distal part are often
connected with surgery. This should be done
within three weeks of injury.

24
Q

what do the macrophages and microglia do after a primary injury

A

Macrophages and microglia will engulf debris and the injury site becomes walled off by a glial scar

25
Q

what chemicals does the glial scar express

A
  • Expresses chemicals that inhibit axon growth – chondroitin sulphate proteoglycans
26
Q

why is the glial scar good and why is it bad

A

GOOD: because it engulfs debris, seals lesion site and repairs
BBB

BAD: physical and chemical barrier for neurodegeneration
(inhibits axon growth).

27
Q

what is the sporting response

A
  • this happens at the glial scar
  • axons will try and grow through glial
    scar but this fails.
28
Q

what are the two main barriers to CNS repair

A

Hostile environment

  • Scar tissue – physical and chemical barrier
  • Myelin – associated inhibitory proteins

Poor regenerative response

29
Q

what are examples of some myelin inhibitor proteins

A

– Nogo protiens, MAG (myelin-associated glycoprotein), Omgp ( oligodendrocyte myelin glycoprotein

30
Q

what are solutions to CNS repair

A
  1. neuroprotection
  2. promotion of axonal regernation
  3. guiding axonal regrowth
31
Q

describe neuroprotection

A

to contain the effects of early trauma, inflammation, and scar formation
Omega-3 polyunsaturated fatty acids

32
Q

describe promotion of axonal regeneration

A

• positive trophic support
Growth factors
Cell / tissue transplantation (olfactory ensheathing cells, Schwann cells, fetal tissue, stem cells)
• counteracting inhibitory influences
Enzymes to target inhibitory proteoglycans
Inhibitory antibodies to target myelin inhibitory proteins

33
Q

describer guiding axonal regrowth

A

to re-establish appropriate connectivities

- Biomaterial scaffolds (nerve guidance channels; hydrogels

Brain and Behaviour (34 decks)

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