Tissue Injury and Repair: The Nervous System Flashcards
Head trauma
axial, rotational and angular energy applied to the brain determine the severity of shear, tensile and compressive forces that cause neuronal and vascular injury
Meninges
dura mater: outermost
mesothelium: between dura and arachnoid
arachnoid: middle layer
subarachnoid space: between arachnoid and pia mater
pia mater: innermost of three layers- right on the surface of the brain
Blood brain barrier
capillary endothelial cells, basement membrane and astrocytic foot processes make up BBB.
formed structurally by tight junctions between endothelial cells.
formed functionally by specialized transport systems in these cells
Different types of hemorrhage
cortical
epidural: laceration of meningeal artery
hemorrhage in subcortical white matter
subdural hemorrhage- laceration of a vein
subarachnoid hemorhage
deep intracerebral hemorrhage
Head truma
concussion: degenerative changes in brainstem nuclei, more severe if repeated– NOT referring to blood
Contusion: more severe impact–> hematoma in subarachnoid space and /or parenchyma
NB: in birds, PM change of pooling in blood of venous sinuses of calvarium (not d/t trauma, doesn’t indicated damage)
Laceration: torn by fractures or penetrating objects including bone fragments or bullets
As a rule: acute nervous system injuries are more disruptive than slowly developing injuries.
nb: melanosis= melanin on brain
in sheep, completely normal; in dog, indicative of subdural hemorrhage
Astrocytes
structural support
part of the BBB
selective transfer of NTs
fluid and ionic homeostasis
uptake of excess NTs
Brain injury
there are very few fibrocytes in brain, so it can’t form scar tissue
limited fibrosis with penetrating brain trauma or around absceses.
Astrocytes are the principle cells responsible for repair and scar formation in the brain=gliosis
gliosis–>increased number of astrocytes
Large defects–> may be persistent cavity
Astrocytes: hypertrophy and hyperplasia in response to injury
Reactive astrocytes=GEMISOCYTIC astrocytes
Long-standing gliosis=more fibrillar
Microglia
make up less than 5% of glial cells (glial cells=non-neuronal cells than maintain homeostasis, form myelin and provide support and production for neurons)
Microglia proliferate after injury and can transform into brain macrophages
Aggregates at small sites of injury= microglial nodules
Gitter cells
=macrophages that have ingested degenerate myelin and other debris e.g. in liquefactive necrotic area
foamy cytoplasm
gitter cells can persist for months
gitter cells are the eventual result of the microglial phagocytosis
Spinal trauma
extrinsic: cars, kicks, crushing, penetrating objects
- extrinsic fractures most common at thoracolumbar junction
Intrinsic: disc prolapse, pathological vertebral fractures (abscesses, neoplasia)
Inter-vertebral disc disease- often most debilitating in thoraco-lumbar segment, as there is little extra-dural space. Also, thoracic cord is protected by conjugal ligaments.
Inter-vertebral disc disease in chondrodystrophic breeds
Degenerative change is geneticall programmed. begins as early as 6 months.
nucleus pulposus replaced by chondroid tissue. Annulus fibrosis placed under increased stress and is degenerating itself. sudden protrusion likely.
can get disc material protroduing into spinal canal and compressing spinal cord.
Hansen’s type I herniation: release of nucleus pulposus fragments into spinal cord.
Inter-vertebral disc disease in non-chondrodystrophic breeds
age-related fibrous (not cartilage) metaplasia of nucleus pulposus–> gradual loss of elasticity
May be noticed clinicall by age 8-10
Increased stress on annulus fibrosis, which protrudes into spinal canal and compresses cord–>Hansen’s type II herniation
Hansen’s type I vs. Hansen’s type II
Type I: release of nucleus pulposus THROUGH the annulus fibrosis into the spinal canal, resulting in spinal cord compression
Type II: protrusion of annulus fibrosis into the spinal canal, resulting in spinal cord compression.
Cervical stenotic myelopathy
narrowing of spinal cord in the neck
horses: malformation or mal-articulation of cervical vertebrae
seen in young, rapidly growing large breeds of horses.
two types of stenotic myelopathy: 1) cervical static stenosis 2) cervical vertebral instability
Cervical static stenosis
narrowing of spinal cord due to bone formation
would NOT be on ddx list in old horses
usually in horses 1-4 years old at C5-C7.
often see on x-ray
Cervical vertical instability
compression of cord occuring because neck is moving around too much “wobblers”
narrowing of spinal canal only occurs when neck is flexed i.e. dynamic–> related to how vertebrae fit together
usually horses 8-18 months of age at C3-C5
Wallerian Degeneration
Result of trauma
follows myelinated, axonal disruption in the brain, spinal cord or nerve
=squence of degeneration and removal of severed axons.
In peripheral nerves: distal segment degenerates and myelin is removed (phagocytosed) (digestion chambers)
Peripheral nerve damage and removal
neuronal body with axon–> axon gets compressed and damaged–> everything distal to point of trauma is phagocytosed.
digestion chamber=gitter cells come in and digest dead cells
axonal spheroids= damaged axons become swollen (may not always see these)
CNS- axons don’t regenerate
Myelin proteins of oligodendrocytes prevent axonal budding (chemically and antigenically different from peripheral nervous system).
Physical: oligodendrocyte arrangement up to 50 axons
No endoneurium (no fibrocytes). (endoneurium=scaffolding)
Even if there could be repair, there would be no scaffolding on which to guide repair. Oligodendrocytes provide myelin sheath for about 50 axons, plus myelin proteins prevent regeneration.
wallerian degeneration: injury–>axonal skeleton disintegrates–> membrane breaks apart–> axonal degeneration followed by degradation of the myelin sheath and infiltration by macrophages (microglia/gitter cells)–> clear debris from degeneration.
Peripheral nerve regeneration
PNS nerves CAN regenerate. Why? 1) dedicated Schwann cell 2) endoneurium that can act as a scaffold should nerve get damaged.
Following damage, schwann cells proliferate and bridge the gap (oligodendrocytes don’t do this).
Must be closely apposed (<10mm). Schwann cells phagocytose myelin, then extrude it. Picked up by macrophages. Distal and proximal segmenets of the axon degenerate.
Proximal stump of axon generates multiple sprouts. One sprout persists and grows distally (1.5mm per day) to re-innervate muscle. If the sprout manages to find that pathway, it can keep growing.
In CNS, myelin and axons degenerate and are removed by micoglial cells.
Once the regenerated axon reaches the end organ (several months), Schwann cells start to produce myelin.
Internodal segments are shorter–> slower conduction along the axon
Regenerated axon is approx 80% of original diameter–> conduction velocity of nerve impulse is slower.
