SCI - 1 intro Flashcards by Jenn Cantilli

what are the most common causes of acquired SCI

MVAs
- then falls

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what is the most common extent of SCI

incomplete tetraplegia

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where does the spinal cord begin and end

extends from medulla oblongata to level of L1-2 disc

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where does the conus medullaris end

terminal end somewhere between T12 and ‘L2
- L 2 is tip

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what is the cauda equina

nerve roots dangling from L 2 thru S5

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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

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where does the SC get it’s blood supply from

1 ant and 2 posterior spinal arteries

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lateral corticospinal tract: innervates and function

ipsilateral

voluntary motion esp of distal limbs

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ventral corticospinal tract: innervates and function

contralateral

axial ms (minimally)

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rubrospinal tract: innervates and function

ipsilateral

motion of UE
especially precise, fine motor mvmts

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vestibulospinal tract: innervates and function

bilateral

posture and balance

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lateral and medial reticulospinal tract: innervates and function

ipsilateral

posture, balance, spinal reflexes, axial and proximal motions

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anterolateral system (spinothalamic, spinoreticular, spinotectal tracts): innervates and function

contralateral

pain, temp, crude touch

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dorsal column: innervates and function

ipsilateral

proprioception, vibration, deep & discriminative touch

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dorsal spinocerebellar: innervates and function

ipsilateral

unconscious proprioception (trunk and LE)

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ventral spinocerebellar: innervates and function

bilateral

unconscious proprioception (trunk and LE)

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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

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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

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what are 7 traumatic mechanism of SCI

flexion
hyper ext
compression
flexion/rotation
shearing
distraction
penetrating

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what is an example of a hyperextension traumatic mechanism of SCI

fall forward and hit chin

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what is an example of a compression traumatic mechanism of SCI

fall and land on feet

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what is an example of a shearing traumatic mechanism of SCI

MVAs

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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

1. ischemia 2. inflammation and edema 3. ion derangement w demyelination of axons 4. neural cell death 5. 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