week 4: neurobiology: spinal cord injury Flashcards
most spinal cord injuries in UK and USA caused by
traffic accident
falls
spinal cord injuries age and gender stats
80%+ males
average age: 41
no valid explanation
quadriplegia
injury affects lower and upper limbs
paraplegia
injury affects lower limbs only
impact of SCI lesion
neurotic death of neurons
severs axons
vascular injury may occur (extravasation of blood)
blood brain barrier may break
release of excitatory amino acids
if blood brain barrier breaks,
leucocytes invasion and release of toxic cytokines
release of excitatory amino acids causes
massive increase in Ca2+
causes excitotoxicity
further damage to cells that may have survived intitial trauma
secondary injury
-can continue to grow for months
-Wallerian degeneration
-triggers second invasion of inflammatory cells
-activated macrophages and microglial invasion
-astrocytes proliferate and hypertrophy: glia limitans (scar)
Wallerian degeneration
process occurs when axons are severed
axons will die back to soma
glia scar
structure that forms around region to try to mend and protect area
forms several weeks after initial injury
formed by astrocytes
proliferation of astrocytes needed
form scar around region to prevent further damage and to restore barrier between blood and spinal cord
produce inhibitory molecules, chemical and physical barrier to regrowth (of axons?)
ectopic sprouting
sprouting of axons
abnormal growth
causes abnormal reflexes
can cause hyper-reflexia and spasticity
reorganisation of nociceptors
reorganization of autonomic circuits
what can reorgnisation of nociceptors cause
chronic pain syndrome
what can reorganisation of autonomic circuits cause
autonomic dysreflexia
dysregulation of autonomic reflexes e.g controlling blood pressure
many of these reflexes are vital for survival
spinal shock
occurs immediatly after injury
complete lack of reflexes
areflexia or hypo-reflexia and flaccid paralysis
weeks after spinal injury
return of segmental reflexes and hyper-reflexia
months after spinal injury
spastic paralysis:
large spasms and clonus
plasticity
structural, physiological, chemical change in CNS
what do denervation and axotomies result in
reorganisation of networks above and below lesion
limited capacity of CNS to repair itself due to:
- limited neurogenisis
- spontaneous failure of CNS axon regeneration
- limited endogenous repair
- insufficient compensatory plasticity
what can we do to help repair
- reduce secondary damage
- enhance growth potential
- eliminate obstacles
- facilitate synaptic reconnectivity
approved pharmacological treatments to help gain function after spinal cord injuries
none
locomotor training
based on principle of neuroplasticity
designed to improve movement and mobility
take advantage of functioning circuits
lumbar spinal cord possesses all necessary circuitry to produce rhythmic coordinated alternating locomotor behaviors
