Injury & Repair of the Nervous System Flashcards
how can nerve damage spread? [4]
how can nerve damage spread? [4]
**nerve damage can spread:
- anterograde degeneration:**
when the axon distal to the site of injury degenerates
- retrograde degeneration: when the proximal segment starts to degenerate) -
through transneuronal degeneration: the death of neurons resulting from the disruption of input from or output to other nearby neurons.
- to the cell body
what does the success of nerve repair depend on? [2]
what does the success of nerve repair depend on? [2]
- severity of initial injury (primary damage)
- extent of secondary damage
what is wallerian degeneration?
Wallerian degeneration is an active process of retrograde degeneration of the distal end of an axon that is a result of a nerve lesion. It occurs between 7 to 21 days after the lesion occurs. After the 21st day, acute nerve degeneration will show on the electromyograph.
what is neurapraxia? [1]
what is axonotmesis?
what is neurotmesis?
which of the following are reversible?
neurapraxia: temporary loss of motor and sensory function due to blockage of nerve conduction (temporary damage to myelin). reversible
axonotmesis: disruption of the axons, resulting from severe crush or contusion. myelin and axon damaged. reversible (epineurium still intact)
neurotmesis: both the axons and nerve sheath are disrupted: 3rd degree damage. myelin and axon AND epineurium damaged. partial recovery possible
after nerve injury:
how does the cell communicate that its injured? [3]
what transformation does cell undergo (in function?) [1]
how does the cell communicate that its injured? [3]
- get a burst of APs (alerts the cell body in DRG that damage has occurred)
- disruption of retrograde transport flow of trophic support (this is a negative injury signal bc its a stop to normal procedure)
- postive injury signals
= all alert DRG that is damaged !!
what transformation does cell undergo (in function?) [1]
cells in the DRG alter their phenotype (switch from transmission of information state to growth state.
how does neuron switch from transmission state to growth state? [2]
- decrease ion channels and proteins involved in NT
- increased proteins involved in axonal growth xx
how does nerve regeneration occur? which cells are involved
the process of nerve regeneration:
- schwann cells divide & secrete trophic factors to attract axon then remyelinate new axons
what is a key determinant in the outcome of repair for nerve injury? [1]
why? [1]
what happens as a result of prelonged muscle denervation? [2]
what is a key determinant in the outcome of repair for nerve injury?
time: prolonged axotomy significantly reduces the number of motorneruons and their axons that can regenerate
because: after one month, schwann cells down-regulate their regeneration asscoated factors
what happens as a result of prelonged muscle denervation? [2]
- muscle atrophy
- decrease in no. of regenarating axons through the deteriorating intra-muscular sheath
spinal cord trauma produces what? occurs from here? [2]
what do macrophages and glial cells make when spinal cord injury occurs? [1]
spinal cord trauma produces what? occurs from here? [2]
site of primary cell death: rapidly spreads into a zone of secondary cell death|
then produces a zone of secondary cell death
(spinal cord injury occurs from both primary and secondary cell death)
macrophages and microglia engulf debri and injury site becomes walled off by a glial scar
what is the role of the glial scar when spinal cord injury is made? [4]
is it a physical or chemical barrier for neuroregneration? [1]
- engulfs debris
- seals lesion site
- repairs the blood-spinal cord barrier
- expresses chemicals that inhibit axon growth
both a physical and chemical barrier for neuroregeneration
what are the two main barriers to CNS repair?
- *1. hostile environment**
i) scar tissue
ii) myelin-associated inhib proteins (NOGO proteins, MAG, OMGP)
2. poor regenerative response (unlike PNS)
how can the we improve spinal cord injury? [3]
- neuroprotection: contain effects of early trauma, inflammation & scar tissue (stop growth of secondary injury / cell death)
-
promotion of axonal regeneration
- positive trophic support
- counteracting inhib influences - guide axonal regrowth to re-establish appropriate connections
CNS treatment:
how does new tech help with
a) promoting axonal regeneration?
b) guiding axonal regrowth?
promoting axonal regeneration:
- removed one olfactory bulbs & took schwann cells & grew in culture
- injected above and below injury site
guiding axonal regrowth:
- scaffold of nerve tissue grafts- bridge the sites of injections
ALSO undergoes loads of rehab
** what changes would be felt bc of this lesion (brown-sequard)? **
- loss of pain and temperature on right side of body below lesion (spinothalamic decussates at level of spinal cord entry)
- loss of motor movement on same side as lesion (corticospinal goes down ipsilateral side)
- loss of proprioception and vibration sense on the same side from damage (DCML has already decussated)
which of the following is best described as ‘tempory blockage of motor and sensory nerve conduction, reversible’
neurapraxia
axonotmesis
neurotmesis
which of the following is best described as ‘tempory blockage of motor and sensory nerve conduction, reversible’
neurapraxia
axonotmesis
neurotmesis
which of the following is neurapraxia?
A
B
C
which of the following is neurapraxia
A
B
C
which of the following is neurotmesis?
A
B
C
which of the following is neurotmesis?
A
B
C
which of the following is axonotmesis?
A
B
C
which of the following is axonotmesis?
A
B
C
