SCI Flashcards

1
Q

what are causes of SCI

A

traumatic = vehicle accidents, acts of violence, falls, sports + recreation
non-traumatic = diseases

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2
Q

describe dorsal column spinal tract

A
  • ascending (sensory) info eg: fine touch, pressure + proprioception
    from spinal cord, to thalamus
    decussation = brainstem
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3
Q

spinothalamic tract

A

ascending (sensory info eg pain, temp, crude touch
from spinal cord, to thalamus
decussation = spinal cord

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4
Q

spinocerebellar tract

A

ascending (sensory) info = proprioception
from spinal cord to cerebellum
decussation = ipsilateral input, direct and indirect pathway, indirect pathway decussates twice

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5
Q

corticospinal (pyramidal) tract

A

descending (motor) info = voluntary control
from cerebral cortex to spinal cord
decussates = brainstem (pyramids)

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6
Q

what are the types of spinal cord injury and mvm
+ common cord injuries

A

mvm = flexion, compression + hyperextension
results from accel/deceleration forces
most common = C1-C2, C4-C6 + T11-L2 (most mobile parts)

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7
Q

describe severity/level of injury based on site

A

cervical (quadriplegia)
- c1-c4 = life threatening diaphragm
- c5-c7 = mvm in neck, shoulders, scpula + inc arm mvm closer to c7
thoracic + lumbar (paraplegia)
- t1-t12 transection injury => paraplegia, t12 can regain ambulation like lumbar and sacral

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8
Q

what is the classifaction of SCI

A

american spinal injury assocation (ASIA)
touch + pinprick sense in each dermatome
test strength of 10 key muscles on each side of body

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9
Q

what is central cord syndrome

A

cervical injuries only
damage = ischaemia, haem, necrosis of central portions of spinal cord
spared = corticospinal tracts
impair = mvm arms + hands

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10
Q

anterior cord syndrome

A

flexion injuries
damage = anterior portion SC/ block blood supply from atnerior spinal artery
spared = dorsal columns (fine touch, vibration, proprioception)
impairment = below injury motor func, pain, temp

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11
Q

brown-sequared syndrome

A

damage = hemisectioned damage exclusively to one lateral side
impair on ipsilat = motor function, dorsal columns
impair on contralat = pain, temp, crude touch bc spinothalamic decussates at spine

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12
Q

what is primary injury

A

contusion, compression, lacerations, shearing stretching
haem in central grey matter, inc in size over time
haem max at injury site, extends towards head and feed

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13
Q

describe secondary injury

A

• Neuropathologic changes - haemorrhage, oedema, neuronal necrosis, axonal
fragmentation, demyelination, and eventually cyst formation
• Vascular changes – ischemia, reduced SCBF, BSCB permeability
• Biochemical alterations - ↑ Na+ & Ca2+↓ K+
, cytotoxic oedema, halt mitochondrial
ATP production.
• Apoptosis
• Excitotoxicity – Glutamate release
• Lipid peroxidation/free radical injury
• Immune response – complement cascade, macrophage infiltration, activated
microglia and astrocytes.

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14
Q

signs and symptoms

A

loss mvm, sensation (heat/cold/touch)
pain
loss bowel/bladder control
inc reflex/spasm
changes to sex function/fertility
difficulty breathing, coughing
age-related defecits bc now have longer life expectancy

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15
Q

what is autonomic dysreflxia

A

50-90% tetraplegics
stim symp nervous system = uncompensate cardio response
hypertension, headache, blurred vision, bradycardia, dilation skin blood vessels, flushing, sweating, congetion, nausea

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16
Q

autonomic dysreflexia causes + treatments

A

impaction of bowels, distention of bladder, pressure sores
remove stimulus, low bp
life threatening

17
Q

management of SCI

A

scene = stabilisation (boards, sometimes pressure sores, hard collars)
hospital = surgery to decompress, pharm + non pharm interventions
rehab = locomotor training

18
Q

early vs late decompression

A

early = shorter hospital stay, less ventilation + pulmonary complications + cost reduce, effect greater in more serious injury
= better than late

19
Q

describe pharm interventions for SCI

A

methylprenisolone - syntethic glucocorticoid (controversial)
- in atni flam cytokine release + reduce lipid peroxidation
- administered with 8 hr post injury, otherwise worse outcomes (gastro haem. resp infect)
riluzole = Na chan block = prevents excitotoxicity
not yet approved

20
Q

what are non pharm interventions for SCI - CSF drainage + MABP augmentation

A

remove V from space around spinal coloumn => dec presh => improve blood flow
inc mabp -> inc perfusion spinal cod
decrease intrathecal presh?

21
Q

what are non pharm interventions for SCI - therapeutic hypothermia

A

buy time
inc healthy tissue in peri-inury region
inc sparrking grey + white matter damage within injury site
improves functional outcome

22
Q

describe some novel regenerative approaches

A

electrical stimulation
delivery nanosystems
cell therapy
biomolecules
bioscaffold

23
Q

what is the prognosis/recovery of SCI

A

heterogeneous = hard to predict outcome
type, severity, incomplete/complete
improvement occurs 6-18months post injury
sometimes deteriorate over time