SCI Flashcards
what are causes of SCI
traumatic = vehicle accidents, acts of violence, falls, sports + recreation
non-traumatic = diseases
describe dorsal column spinal tract
- ascending (sensory) info eg: fine touch, pressure + proprioception
from spinal cord, to thalamus
decussation = brainstem
spinothalamic tract
ascending (sensory info eg pain, temp, crude touch
from spinal cord, to thalamus
decussation = spinal cord
spinocerebellar tract
ascending (sensory) info = proprioception
from spinal cord to cerebellum
decussation = ipsilateral input, direct and indirect pathway, indirect pathway decussates twice
corticospinal (pyramidal) tract
descending (motor) info = voluntary control
from cerebral cortex to spinal cord
decussates = brainstem (pyramids)
what are the types of spinal cord injury and mvm
+ common cord injuries
mvm = flexion, compression + hyperextension
results from accel/deceleration forces
most common = C1-C2, C4-C6 + T11-L2 (most mobile parts)
describe severity/level of injury based on site
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
what is the classifaction of SCI
american spinal injury assocation (ASIA)
touch + pinprick sense in each dermatome
test strength of 10 key muscles on each side of body
what is central cord syndrome
cervical injuries only
damage = ischaemia, haem, necrosis of central portions of spinal cord
spared = corticospinal tracts
impair = mvm arms + hands
anterior cord syndrome
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
brown-sequared syndrome
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
what is primary injury
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
describe secondary injury
• 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.
signs and symptoms
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
what is autonomic dysreflxia
50-90% tetraplegics
stim symp nervous system = uncompensate cardio response
hypertension, headache, blurred vision, bradycardia, dilation skin blood vessels, flushing, sweating, congetion, nausea
autonomic dysreflexia causes + treatments
impaction of bowels, distention of bladder, pressure sores
remove stimulus, low bp
life threatening
management of SCI
scene = stabilisation (boards, sometimes pressure sores, hard collars)
hospital = surgery to decompress, pharm + non pharm interventions
rehab = locomotor training
early vs late decompression
early = shorter hospital stay, less ventilation + pulmonary complications + cost reduce, effect greater in more serious injury
= better than late
describe pharm interventions for SCI
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
what are non pharm interventions for SCI - CSF drainage + MABP augmentation
remove V from space around spinal coloumn => dec presh => improve blood flow
inc mabp -> inc perfusion spinal cod
decrease intrathecal presh?
what are non pharm interventions for SCI - therapeutic hypothermia
buy time
inc healthy tissue in peri-inury region
inc sparrking grey + white matter damage within injury site
improves functional outcome
describe some novel regenerative approaches
electrical stimulation
delivery nanosystems
cell therapy
biomolecules
bioscaffold
what is the prognosis/recovery of SCI
heterogeneous = hard to predict outcome
type, severity, incomplete/complete
improvement occurs 6-18months post injury
sometimes deteriorate over time
