Topic 19: Spinal Cord Injury Flashcards

1
Q

What is the Edwin Smith Papyrus?

A

recognized that when injury occurs to the spinal cord it is very bad and cannot be treated

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2
Q

How does the area of damage determine how the person is impaired?

A

deficits are determined by where the injury occurs

every level of the spinal cord has a different function

if damage is here, everything below T1 is disrupted

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3
Q

What is the spinal cord?

A

sensory input via dorsal roots

motor input via ventral roots

dorsal root ganglia contain cell bodies of sensory afferents (posterior to humans)

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4
Q

What are the nerve tracts in the spinal cord?

A

dorsal columns: touch, proprioception, vibration

spinocerebellar: movement regulation, balance communicates to the cerebellum

spinothalamic: temperature, pain, pain signals make synapses with gray matter

reticulospinal/vestibulospinal: walking and posture, initiating movements

corticospinal: voluntary movement, finer movements

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5
Q

What are the ascending tracts in the spinal cord?

A

dorsal columns

spinocerebellar

spinothalamic

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6
Q

What are the descending tracts in the spinal cord?

A

corticospinal

reticulospinal/vestibulospinal

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7
Q

What are projections of major motor and sensory tracts?

A

left motor cortex controls our right hand

muscles, touch/proprioception cross over in the dorsal column nuclei

pain projections cross over to the other side of the spinal cord right away (right as they enter)

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8
Q

What is Brown-Sequard syndrome?

A

lateral hemisection results in loss of temperature and pain sensation and motor function on opposite sides (half of his spinal cord is deficit)

impaired movement same side as injury

impaired proprioception, vibration, 2-point discrimination, and joint and position sensation of the same side as injury

impaired temperature and pain sensation on opposite side

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9
Q

What are the needs of spinal cord injury patients?

A

recognized they wouldn’t be able to walk again, just wanted everyday things back

independent respiration

bladder/bowel control

sexual function

freedom from pain, hypertonus, and spasms

arm and hand function

trunk posture

standing

walking

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10
Q

What are the most common spinal cord injury?

A

bruising, stretching, and compression of spinal cord most common injuries

rarely severed

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11
Q

What is rating chart American Spinal Injury Association (ASIA)?

A

asses what functions are gone and which remain

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12
Q

What are the five levels of the ASIA impairment scale?

A

A: complete, no motor or sensory function is preserved in sacral segments S4-S5

B: incomplete, sensory but not motor function is persevered below the neurological level and includes the sacral segments S4-S5

C: incomplete, motor function is preserved below the neurological level, and more than half of key muscle below the neurological level have muscle grade less than 3

D: incomplete, motor function is persevered below the neurological level, and at least half of key muscles below the neurological level have a muscle grade of 3

E: normal, motor and sensory function are normal

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13
Q

What does paraplegic mean?

A

impairment of legs and lower trunk

impairment of bladder, bowel, and sexual function

lower down, arms and neck are fine

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14
Q

What does quadriplegic or tetraplegic mean?

A

high C or T area

partial or total loss of function in limbs and torso

impairment of bladder, bowel, and sexual function

may be unable to breath is damage is in neck region (segments C1-C5)

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15
Q

What are additional complications of spinal cord injury?

A

development of hyperactive reflexes and spasms

autonomic dysreflexia

loss of bladder and bowel control

pressure ulcers

neuropathic pain weeks/months after injury

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16
Q

How does intrathecal baclofen treat spasticity?

A

intrathecal: administered into spinal canal

brain cannot get signals to regulate functions out

baclofen is a GABA-B receptor agonist

increases presynaptic inhibition of transmission from sensory afferents

bathes spinal cord with drugs

sensory input is able to occur, just can’t be controlled by brain

baclofen can be given orally for mild spasticity

17
Q

What is autonomic dysreflexia?

A

uncontrollable and dangerous

extended bladder activates sympathetic division of the autonomic nervous system

results in dangerously high blood pressure that is not compensated by central inhibition to the heart

need to regulate sympathetic responses

18
Q

Why is control of bladder and bowel function often lost in spinal cord injury?

A

coordination of autonomic and somatic responses for normal bladder function require neural networks in the brain stem

signal from brain to relax muscles to pee never comes, which causes sympathetic activation

19
Q

What immediate treatments for spinal cord injury?

A

immobilization

sometimes spinal surgery to decompress cord, remove bone fragments, and align vertebra

drugs to reduce swelling and inflammation

rehabilitation: get them moving again and re-training motor circuit

20
Q

What is secondary damage in spinal cord injury?

A

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

initial lesions increase in size and cause more cell death

21
Q

What are the factors involved in secondary damage?

A

ischemia: reduced oxygenation of tissue, compression causes blocked oxygen flow

edema: swelling with inflammation

glutamate increase: neuro-toxic, too much excitation is not a good thing

blood brain barrier breakdown: breaks down because of trauma, lets undesirable things in

inflammation: invasion from macrophages, activation of microglia

22
Q

What is the evidence for rhythmic networks in human spinal cord?

A

electrical stimulation of spinal cord in SCI patient evokes rhythmic activity in leg muscles: stimulate healthy neurons without the use of the brain

electromyograms

23
Q

What is a LOCOMAT?

A

a commercial device to improve walking

treadmill therapy can improve walking

24
Q

What are the goals of future possibilities of treatment of spinal cord injury?

A

to repair the damaged spinal cord

to enhance plasticity of undamaged neurons (form new connection from existing connections)

25
Q

Why do damaged axons in the CNS not regenerate?

A

growth inhibitors on CNS myelin: the environment limits growth, wants to prevent unregulated growth (cancer)

mechanical barriers: scar tissue, physical barriers like glial scars, scar formed around injury site to protect and prevent spreading

need to get around these things while keeping the benefits

26
Q

What are two treatment strategies currently under investigation?

A

promoting regeneration of damaged axons: blocking growth inhibitory molecules (neutralize inhibition), bridging damaged regions (scaffolding), digesting scar tissue (best start)

enhancing the function of existing nerve cells: promote function of things left behind, remyelinate axons, promote “sprouting” (new growth on existing factors)

27
Q

What are growth inhibitory molecules?

A

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

28
Q

What are some examples of growth inhibitory molecules?

A

Nogo-A

myelin associated glycoprotein (MAG)

oligodendrocyte myelin glycoprotein (OMgp)

chondroitine sulphate proteoglycans (CSPGs)

29
Q

How are growth inhibitory factors blocked?

A

apply antibodies to block inhibitors on myelin or their receptors on growth cones

tested for Nogo on oligodendrocytes

anti-Nogo currently in clinical trials

30
Q

How is the lesion site bridged?

A

put in scaffolds to make environment more favorable to growth

mechanical bridges: inorganic and organic material

Schwann cells: myeline producing cell in peripheral nerves, support growth

olfactory ensheathing cells: glia from olfactory bulb

stem cells: to produce growth promoting environment, can become any type of cell

31
Q

How can the glial scar be digested?

A

CSPG: chondroitin sulfate proteoglycan, part of the extracellular matrix, upregulated by astrocytes after injury

for example: apply the enzyme chondroitinase, clip away or cut CSPG at particular sites, like trimming a shrub

32
Q

How can axons that have been demyelinated after injury be remyelinated?

A

use for stem cells engineered to produce oligodendrocytes

turn stem cells into glial cells is easier than turning them into neurons

clinical trail for stem cell therapy for remyelination started but stopped (too costly for little return)