SCI - 1 intro Flashcards
what are the most common causes of acquired SCI
MVAs
- then falls
what is the most common extent of SCI
incomplete tetraplegia
where does the spinal cord begin and end
extends from medulla oblongata to level of L1-2 disc
where does the conus medullaris end
terminal end somewhere between T12 and ‘L2
- L 2 is tip
what is the cauda equina
nerve roots dangling from L 2 thru S5
how will a SCI present above vs below conus medullaris/L2
above: CNS
- UMN s/sx w inc tone and refelxes
below: PNS
- LMN s/sx w low tone, hyporeflexia
where does the SC get it’s blood supply from
1 ant and 2 posterior spinal arteries
lateral corticospinal tract: innervates and function
ipsilateral
voluntary motion esp of distal limbs
ventral corticospinal tract: innervates and function
contralateral
axial ms (minimally)
rubrospinal tract: innervates and function
ipsilateral
motion of UE
especially precise, fine motor mvmts
vestibulospinal tract: innervates and function
bilateral
posture and balance
lateral and medial reticulospinal tract: innervates and function
ipsilateral
posture, balance, spinal reflexes, axial and proximal motions
anterolateral system (spinothalamic, spinoreticular, spinotectal tracts): innervates and function
contralateral
pain, temp, crude touch
dorsal column: innervates and function
ipsilateral
proprioception, vibration, deep & discriminative touch
dorsal spinocerebellar: innervates and function
ipsilateral
unconscious proprioception (trunk and LE)
ventral spinocerebellar: innervates and function
bilateral
unconscious proprioception (trunk and LE)
where does information in the lateral corticospinal tract cross and what does this mean for SCIs
crossed in pyramids
SCI will mean an ipsilateral loss of voluntary motion of distal limbs if damage in the SC
describe the anatomy behind how pinprick sensation is a good prognosticator for ambulation
lateral spinothalamic tract detects pain, so if can detect pinprick, tract is intact
lateral corticospinal tract = voluntary motion
literature says that if tract/sensation is intact below the level of SCI, inc likelihood of amb bc of close proximity of spinothalamic to lateral corticospinal tract
–> inc likelihood of resolution of edema and swelling and preservation of corticospinal tract –> regaining strength
what are 7 traumatic mechanism of SCI
flexion
hyper ext
compression
flexion/rotation
shearing
distraction
penetrating
what is an example of a hyperextension traumatic mechanism of SCI
fall forward and hit chin
what is an example of a compression traumatic mechanism of SCI
fall and land on feet
what is an example of a shearing traumatic mechanism of SCI
MVAs
what is an example of a distraction traumatic mechanism of SCI
pulled axillarily
what is an example of a penetrating traumatic mechanism of SCI
GSW
stab wounds
what are 5 factors that impact traumatic patterns of bony ligamentous damage in a SCI
body position
magnitude
rate of application
duration of force
point of force application
what are the 2 most vulnerable areas of the spinal cord and why
C5-7
T12-L2
changes in angle so inc chance of moving and injury
why are SCI most common in the cspine
poor mechanical stability
- not well supported by ms
- lot of mobility
what are the 3 most common causes of a SCI in the tspine
gunshot wounds
MVA
falls
rank the spines in order of stability
most
tspine
lumbar
cspine
least
how vulnerable is the tspine to SCI and what does this often mean for tspine SCI
very stable bc of ribs, highly protected
only see damage if severe force of magnitude
- if damaged more likely to be complete
- if incomplete - GSW, stab wounds
what are the 4 most common causes of lumbar SCIs
falls
MVA
gunshot wounds
crush injuries
how vulnerable is the lumbar to SCI and why
intermediate level of stability d/t strong ms around it
what are 6 non traumatic causes of SCIs
spinal hematoma
infection
radiation
neoplasm
vascular interruption
rheumatoid arthritis
how can a spinal hematoma lead to a SCI
blood is toxic to nervous system
- also taking up space –> compression on SC
how can radiation lead to a SCI
impacts neurologic tissue
how can a neoplasm lead to a SCI
carcinogenic tissue can cause injury to nerves and SC
what are types of vascular interruptions that can lead to a SCI
ischemia
hemorrhage
how can RA lead to a SCI
bony changes
why do you typically see a combo of presentations with SCI
not typical to have SCI in one area of spine
also more common for SCI to be incomplete
what are 5 incomplete SCI syndromes
central cord
anterior cord
brown-sequard
conus medullaris
cauda equina
central cord syndrome: typical cause, location, and pt pop
hyper extension injury –> crush and damage central part of SC from bleeding into central gray matter
cspine
older individuals w spinal stenosis / narrowing of canal
- more likely to see damage w hyper ext
how does central cord syndrome typically present and why
UE more involved than LE
- d/t topographical orientation of homunculus (corticospinal UE more medial and LE more lateral)
impacting corticospinal (pinprick, strength of UE) and DCML (proprioception in both UE and LE) –> could still have 5/5 strength of LE
what is the typical cause of anterior cord syndrome
flexion injury and teardrop fxs
how does anterior cord syndrome typically present
loss of motor function and pain/temp sensation below injury
what is the prognosis for anterior cord syndrome
poor for amb as corticospinal tract is hit
poor for bowel and bladder
brown-sequard syndrome: what is damaged, how does it present
1/2 of SC damaged
ipsilateral proprioception and motor loss
contralateral loss of pain/temp sensation
conus medullaris syndrome: what is damaged, presentation
injury of sacral cord (conus)
combo of UMNL and LMNL signs bc b/w central and peripheral
motor and sensory loss in LEs
areflexic bladder/bowel
cauda equina syndrome: what is damaged, presentation
injury to lumbosacral nerve roots (LMNL)
LMNL bc more peripheral
- flaccid paralysis
- “saddle” paresthesia
- areflexic bladder/bowel
what often causes the most damage to the SC
secondary sequelae of initial trauma
what are 5 mechanisms of secondary tissue destruction
- ischemia
- inflammation and edema
- ion derangement w demyelination of axons
- neural cell death
- necrosis / apoptosis (necrosis replaced by scarring and cysts)
what is spinal shock
transient physiological phenomenon
- sx in the first minutes to hours up to 1st week after trauma
depression or loss of SC function below level of injury (reflex arcs, motor, sensory, autonomic function) until reflex arcs below level of injury begin to function again
- loss of bulbocavernosus refelx, DTRs
- doesn’t imply state of circulatory collapse
- returns sooner in incomplete
eventually anything neurologically intact wakes up
what influence does neurogenic shock have
impacts sympathetic ANS
does the SC have to be severed for irreversible damage
no
- secondary sequelae can cause a lot of irreversible damage
what is neurogenic shock
disruption of sympathetic nervous system outflow from T1-L2 leading to dec in vascular resistance w associated vascular dilation
- preserved parasympathetic system functioning
what level of injury is neurogenic shock typically seen in and why
in injuries above T6, more in tspine levels
that is where the sympathetic nervous system lives
- parasympathetic lives in brain so that is why that function is often preserved
neurogenic shock presentation and why
HoTN
- can get lifethreatening low
bradycardia
hypothermia
sx are based on blood flow in body that is diminished
can be life threatening
how long do neurogenic shock sx last
up to 4-5wks
