SCI Flashcards
What spinal levels have the greatest frequency of injury?
C5
C7
T12
L1
Describe the pathophysiology of a spinal cord injury, either traumatic or non.
primary injury: interruption of blood supply
secondary injury: ischemia, edema, demyelination, necrosis of axons, progressing to scar tissue formation
Provide some non-traumatic causes of SCI.
disc prolapse, cancer, vascular insult, infection
For a C7 lesion, what level would you expect to see motor deficits?
C8 and below
- lesion level indicates most distal segment with preserved motor function (3+5 and above)
Paraplegia results from SCI at what levels?
T1 to L1, involving BLEs and trunk at varying levels
Your patient is an ASIA C - what can you expect about motor/sensory function?
C = incomplete -> motor is preserved below neuro level, and most key muscles are < 3/5
Describe the ASIA scales of SCI.
A = complete B = sensory but not motor function is preserved below neuro level and includes the sacral segments S4-5 C = motor is preserved below neuro level, but most muscles are < 3/5 D = motor is preserved below neuro level, and most muscles are >3/5 E = motor and sensory is normal
remember, sensory BEFORE motor
Central cord syndrome is commonly caused by what mechanism? What areas of function are preserved?
- caused by hyperext. injuries to c-spine
- preservation of more peripherally located lumbar/sacral tracts/leg fxn
- proprioception/sensory descrim preserved
Which areas are lost with central cord syndrome?
lost:
- bilat spinothalamic (medial tracts in cord)
- ventral horn with BUE loss
What is Brown-Sequard syndrome?
hemisection of spinal cord typically d/t penetration wounds (bullet, knife)
asymmetrical symptoms
Your patient has a R T11 Brown-Sequard SCI. Describe the motor and descrim touch changes he likely has.
R T11 lesion
DCML: ipsilateral
- R loss of descrim touch/proprioception at T11 and below (ispsilateral b/c info can’t get up past the lesion to cross in medulla)
CST: ipsilateral
- LMN symptoms at R T11 (LMN cant get out to area)
- UMN symptoms at R T12 and below (UMN can’t get down to synapse onto LMN at indiv. levels)
Describe the pain/temp changes that occur in a brown-sequard syndrome at R T11 lesion.
R T11 lesion
SPINOTHALAMIC: contralateral/ipsi
- L loss of pain/temp from T12 and below (these tracts from the L have already crossed midline, so they’re on the R side now, and then they course up and hit the lesion.. so no more info)
- R loss of pain temp at T11 (the T12 tract courses up and hits the roadblock at T11, hasn’t crossed midline yet so you get ipsilateral pain/temp loss at lesion level)
Anterior cord syndrome is primary caused by what mechanism? What functions are preserved, and what are lost?
- caused by hyperflexion at C-spine
- bilateral: lost motor function, pain/temp, spastic paralysis below level
- preserved light touch/proprioception
In posterior cord syndrome, what is lost and what is preserved?
lost: DCML
preserved: CST/STT
VERY RARE
Describe bowel/bladder ability for cauda equina syndrome.
flaccid paralysis of bladder/bowel
What vertebral level does the injury occur in cauda equina syndrome? What results?
injury below L1
- results in injury to lumbar/sacral roots of peripheral nerves with sensory loss and paralysis
- flaccid motor paralysis with no spinal reflex activity
If a patient has “sacral sparing”, what does this mean?
sparing of tracts to sacral segments, with preservation of perianal sensation, rectal sphincter tone, or active toe flexion
T/F: Cauda requina is reversible.
true, nerve regeneration can occur but is often incomplete
- slows and stops after ~ 1yr
In SCI lesions above C4, what is especially important to examine?
respiratory function
- phrenic nerve, C3-5, innervates the diaphragm
Describe the scoring of the modified ashworth.
0 =
1 = slight catch and release, or resistance at end of ROM
1+ = catch, but followed by resistance in < half of ROM
2 = Resistance through > half ROM, but limb still easily moved
3 = considerable tone increase, PROM difficult
4 = limb completely rigid, no passive movement able
How long does spinal shock last?
flaccidity/reflex depression = can last for several hours or up to 24 weeks (?? online says 6, book says 24)
What is autonomic dysreflexia? Symptoms?
noxious stimulus (kinked catheter, tight clothes, ulcer, positioning) precipitates a pathological autonomic reflex with symptoms of:
- paroxysmal hypertension (stress/event induced)
- bradycardia
- diaphoresis, flushing, headache
- convulsions
What are your first steps when treating autonomic dysreflexia?
elevate head, check and empty catheter first
You suspect your patient of having heterotopic bone formation. How might you suspect this?
soft tissue swelling, pain, erythema - generally near a large joint
