Spinal Cord Injury Flashcards
vertebral column
divided into vertebral bone segments fused together
protects the spinal cord
Cervical, thoracic, lumbar, and sacral spinal levels
an injury leads to loss of function of everything below the level it occurs at
spinal nerves
run through the vertebra and correspond to the level of spinal cord
divided into different functions
cervical - vital autonomic functions
thoracic - regulating sympathetic nervous system
lumbar - lower body movements
sacral - sexual function
dermatome
region of body surface that corresponds to a spinal segment - related to spinal nerves
strips of innervation and ennervation territory
spinal cord
sensory input via dorsal roots
motor output via ventral roots
dorsal root ganglia contain cell bodies of sensory afferents
nerve fibre tracts in spinal cord
descending:
- corticospinal tracts
- reticulospinal/vestibulospinal tracts
ascending:
- dorsal columns
- spinocerebellar tracts
- spinothalamic tracts
dorsal columns
ascending tract - sensory info
touch, proprioception, vibration
spinocerebellar tracts
ascending tract - sensory info
movement regulation
sense of balance - project to cerebellum
spinothalamic tracts
ascending tract - sensory info
temperature + pain
neurons synapse with neurons in grey matter of dorsal horn → crossed pathway
corticospinal tracts
descending - motor output
voluntary movement
finer movements
reticulospinal/vestibulospinal tracts
descending - motor output
walking and posture
movement initiation
info comes from brain stem - reticular formation
pain/temperature projection
crossed pathway = information enters spinal cord and makes connections to cell → axon immediately crosses over and ascends to thalamus and then projects to sensory cortex
(left side input → right side of spinal cord → right thalamus → right sensory cortex)
touch/proprioception projection
ascends ipsilaterally = makes first synaptic contact in dorsal column → those nerves will then cross over to thalamus → sensory cortex
(left side input → left dorsal column nuclei → cross to right thalamus → right sensory cortex)
muscle motor projection
info descends from motor cortex → crosses over to opposite side → spinal cord
left motor cortex controls right side motor actions
Brown Sequard syndrome
lateral hemisection → impaired pain/temp on opposite side; impaired motor function + proprioception on same side
injury to left side interrupts the connection = no perception of pain/temp from right side; no movement or proprioception on left side
spinal cord injury
most common = young men (16-30)
vehicle accidents, violence, falls, sports
injury rarely severs spinal cord; more commonly bruised, stretched, or compressed → crushed column - pieces break off and embed in tissue
needs of SCI patients
freedom:
independent respiration
bladder/bowel function
sexual function
freedom from pain/spasms
arm/hand function
trunk posture
standing
walking
ASIA classification of SCI
standard rating - allows assessment of deficits and remaining function
loss of sensory and motor function
5 levels: A = complete loss → E = normal function
paraplegic
lower damage = impairment of legs, lower trunk, bladder + bowel, sexual function
quadriplegic
partial or total loss of function in all limbs and torso
impairment of bladder, bowel, + sexual function
if injury to cervical level - impaired breathing
additional complications
paralysis is immediate effect
1. hyperactive reflexes and spasms
2. autonomic dysreflexia
3. loss of bladder and bowel control
4. pressure ulcers
5. neuropathic pain
Baclofen
administered intrathecally (into spinal canal) to reduce severe spasticity (or orally for mild)
GABA-B receptor agonist
increases presynaptic inhibition of transmission from sensory afferents
impaired descending inhibition column → add inhibition back
autonomic dysreflexia
extended bladder activates sympathetic division of ANS → high blood pressure - not compensated for by central inhibition to heart = dangerous
descending brain activity regulation is impaired
can treat by interrupting control to inhibitory systems to shut off SNS and get PNS
loss of bladder and bowel control
coordination of autonomic and somatic responses required neural networks in brain stem
stretch of bladder activates afferents → signal to PNS to contract bladder
sphincter muscles cannot be uninhibited because there is no brain signal
immediate treatments for SCI
- immobilization - prevent further damage
- spinal surgery to decompress cord - return to normal alignment
- drugs to reduce inflammation - cascade effect on nearby cells can be prevented
- rehabilitation - retraining motor circuits
secondary damage in SCI
increase in cell death and demyelination following initial injury
wave of inflammation/cascade to cells in surrounding tissues
- ischemia (reduced oxygen)
- edema (swelling)
- glutamate increase (cell death causes burst of excitation)
- BBB breakdown (trauma)
- inflammation (invasion from macrophages; activation of microglia)
rhythmic networks in spinal cord
electrical stimulation of spinal cord in SCI patient evokes rhythmic activity in leg muscles
spinal cords have inherent rhythmicity → use central pattern generators to trigger
movement by bypassing brain
rehab therapies
treadmill therapy - improve walking
LOCOMAT
future possibilities
goal: repair damage + enhance plasticity of undamaged neurons → grow new connections from existing
axons in CNS
damaged axons in CNS do not regenerate
1. growth inhibitors on CNS myelin = limit to prevent uncontrollable growth
2. mechanical barriers = form after injury to protect area
glial scar
glial cells from scar around injury site
serves protective function - damage can’t spread
axon cannot regrow on glial scar
treatment strategies
- promote regeneration of damaged axons
- block growth inhibitory molecules
- bridge damaged regions
- digest scar tissue - enhance function of existing nerve cells
- remyelinate axons
growth inhibitory molecules
myelin: - Nogo-A, MAG, OMgp
CSPGs
any growth will retract backwards from molecules
apply antibodies to block inhibitors on myelin or their receptors on growth cones
CSPGs
chondroitin sulfate proteoglycan
part of extracellular matrix
main growth inhibitor
bridging lesion
- mechanical bridges
- Schwann cells - myelin-producing cells in periphery
- olfactory ensheathing cells - glia from olfactory bulb; promotes axon growth (like stem cells)
- stem cells - produce growth promoting environment
digest scar tissue
CSPG is upregulated after injury by astrocytes
applying enzyme chondriotinase will cut CSPG in particular sites so axons can grow through
remyelination of axons
use stem cells to produced oligodendrocytes - glial cells
will remyelinate damaged axons + improve residual function
