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Neuro 210 > Spinal Cord Injury > Flashcards

Spinal Cord Injury Flashcards

1
Q

What was the oldest ever written observation on spinal cord injury in egypt?

A

the Edwin Smith Papyrus claimed that soldiers with spinal cord injuries lost most basic functions and COULD NOT RECOVER

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2
Q

What are the most important spinal cord levels?

A

the cervical region at the head, if damaged can cause respiratory and heart rate problems

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3
Q

What are the 3 Ascending (going to brain) nerve fiber tracts in the spinal cord?

A
  1. Dorsal Columns include information on touch, proprioception and vibration (transferes large diabeter A-beta fibers)
  2. Spinocerebellar tract –> sends info on movement regulation to cerebellum
  3. spinothalamic tract –> sends info on temperature and pain –> mainly A-delta and c- fibers prject into the spinal cord dorsally and make a synapse and go out the other end
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4
Q

what are 2 decsending (from the brain) nerve fiber tracts in the spinal cord?

A
  1. Corticospinal —> delivers info on voluntary movement (critical for fine movement)
  2. reticulospinal/vestibulospinal –> walking and posture movements
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5
Q

Where does the sensory input go to in the spinal cord?

A

goes to the dorsal roots/ posterior roots

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6
Q

Where does the motor neurons leave the spinal cord?

A

ventral/anterior roots

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7
Q

What are the dorsal root ganglia

A

contain cell bodies of sensory afferents

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8
Q

What is brown-sequard syndrome?

A

its a lateral hemisection that results in loss of temperature and pain sensation and motor function on the opposite sides

  • any pathway thats ipsilateral will cause an deficit on the same side as injury
  • any pathway that is contralateral will cause a deficit in the opposite side as the injury
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9
Q

What is hemisection

A

its when half of the spinal cord is injuried unilaterally

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10
Q

What pathways are ipsilateral?

A

the proprioception and touch

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11
Q

what pathways are contralateral?

A

pain and temperature and movement

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12
Q

Why is propriception ipsilateral and pain and temp + movement/muscles are contralateral?

A

because pain and temperature cross over in the spinal cord and propioception crosses over later on in the medulla

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13
Q

what is 80% of spinal cord injury caused by?

A

car crashes, diving accidents..etc..

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14
Q

What is the scale used to rate spinal cord injury levels and what are the 5 types of levels it has?

A

called the Rating chart American Spinal Injury Association (ASIA) and it has 5 levels from A to E where A and B are the most severe ratings and C,D and E are less severe
- useful for rehab assessments

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15
Q

What are the 2 groups that spinal cord injury patients are generally divided into?

A
  1. paraplegic: impairement of legs and lower trunk along with impairement of bladder, bowel and sexual function
  2. quadriplegic –> partial or total loss of function in limbs and torso, impairement in bladder, bowel and sexual function, may be unable to breathe if damage is in neck/cervical regions
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16
Q

What are 5 additional complications of spinal cord injury?

A
  1. Development of hyperactive reflexes and spasms (arises when our brain is cut from the spinal cord due to injury and theres no regulation of movement from the brain)
  2. autonomic dysreflexia (complete general inhibition unless excited by brain)
  3. loss of bladder and bowel control
  4. pressure ulcers (form because they sleep in the same position for hours without movement whch causes ulcers in butt and legs)
  5. neuropathic pain weeks/months after injury (due to nerve damage)
17
Q

What is the intrathecal baclofen?

A

it is used to reduce the severe spasticity of individuals with SCI.

  • it is administered into the spinal cord
  • Baclofen is a GABA receptor agnoist (increases gaba levels in spinal cord to help inhibit the transmission from sensory afferents
18
Q

What is autonomic dysreflexia?

A
  • when you have general inhibition of a motor system unless ur brain tells u to excite it (this is a problem in SCI)
  • Extended bladder (when its filled up) activates sympathetic division of the autonomic nervous system and results in dangerously high blood pressure that is not compensated by central inhibition to the heart

the muscles of the bladder are being inhibited and constricted by somatic and sympathetic control and without the brainstem its hard for someone to get help

19
Q

What is the most common injury that occurs within the spinal cord?

A

bruising, stretching and compression of SC after injury; the cord doesnt snap in half, it just gets bruised and bone fragements from the vertebrae will break and press down on the vertebrate tissue

20
Q

What are 4 immediate treatments for SCI?

A
  1. immobilization: implainting a device to decompress and stabilize the spine so it doesnt move around and cause more damage
  2. sometimes, spinal surgery to decompress cord, remove bone fragements and align the vertebrate (stretching tissue and then realigning it)
  3. drugs to reduce swellikng and inflammation
  4. rehab (weeks and months after injury)
21
Q

What is secondary daamge in SCI?

A

increase in cell death and demyelination in days/weeks following primary injury

22
Q

What are 5 factors involved in secondary damage?

A
  1. ichemia
  2. edema
  3. glutamate increase
  4. blood brain barrier breakdown
  5. inflammation (causes further damage of healthy tissue)
23
Q

What are the rhythmic networks in a human spinal cord?

A

called central pattern generators (CPG’s)

  • electrical stimulation of the SC in SCI patient evokes rhythmic activity in the muscle shown in electromyograph
  • this can be useful in walking patterns without brian use
24
Q

what is a LOCOMAT?

A

a device used to improve walking among SCI patients

25
Q

What therapy is done to promote walking in SCI patients?

A

called treadmill therapy

26
Q

What are the goals of future possibilities in terms of treatment of SCI?

A
  1. to repair the damaged SC

2. to enhance plasticity of undamaged neurons (taking other connections and using those to promote functional recovery)

27
Q

What are two causes of why damaged axons in CNS do not regenerate?

A
  1. growth inhibitors on CNS myelin (myelin has a number of factors that limit and shut down regenerative responses by cells in CNS)
  2. Mechanical barriers like scar tissues (physically block axonal growth and cause collapse)
28
Q

What are some growth inhibitory molecules given out by myelin?

A
  • molecules on CNS myelin or extracellular matrix that prevent growth cone extension

1) Nogo-A
2) MAG
3) OMgp
4) CSPG’s (from glia in the extracellular matrix walls; very inhibitory)

29
Q

What are 3 things we can do to promote regeneration of damaged axons?

A
  1. blocking growth inhibitory molecules
  2. blocking damaged regions
  3. digesting scar tissue
30
Q

What are 2 ways we can enhance the function of existing nerve cells?

A
  1. remyelinate axons

2. promote sprouting

31
Q

How can we block growth inhibitory molecules?

A

by applying antibodies to block inhibitors on myelin or their receptors on growth cones (i.e antibody that blocks the nogo-A receptor on the growth cone)

32
Q

What is a way we can block damaged regions so axon growth cones can cross over?

A

by bridging the lesion site

33
Q

what are 5 methods of bridging lesion site to block damaged regions?

A
  1. mechanical bridges (inorganic and organic materials)
  2. schwann cells (myelin in PNS)
  3. olfactory ensheathing cells (glia from olfactory bulb)
  4. stem cells (to produce growth promoting environment)
34
Q

What is one way we can digest scar tissue?

A

to apply the enzyme chondroitinase that attacks the CSGP’s made by astroglia and digest scar tissue

35
Q

What does CSPG’s do to glial scars?

A
  • around lesion cavity, is astrocytes which form and seals off area of damage
  • astrocytes are highly reactive around injury sites and will give out CSPG’s (growth inhibitors) and form glial scars and extend to the outside of the injury to form an extracellular barrier causing all potential regrowing axons to collapse
36
Q

How do we remyelinate axons demyleinated by injury?

A

we use stem cells that are engineered to produce oligodendrocytes

37
Q

how do we enhance plasticity of undamaged neurons?

A

promote sprouting in neurons who are ABOUT to grow
- and potentially increase cAMP levels in undamaged neurons so they can not be further damaged and increase plasticity of neuron so it can take on other functions

Neuro 210 (12 decks)

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