Tissue Injury and Repair: The Nervous System

Question 1

Head trauma

Answer 1

axial, rotational and angular energy applied to the brain determine the severity of shear, tensile and compressive forces that cause neuronal and vascular injury

Question 2

Meninges

Answer 2

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

Question 3

Blood brain barrier

Answer 3

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

Question 4

Different types of hemorrhage

Answer 4

cortical

epidural: laceration of meningeal artery

hemorrhage in subcortical white matter

subdural hemorrhage- laceration of a vein

subarachnoid hemorhage

deep intracerebral hemorrhage

Question 5

Head truma

Answer 5

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

Question 6

Astrocytes

Answer 6

structural support

part of the BBB

selective transfer of NTs

fluid and ionic homeostasis

uptake of excess NTs

Question 7

Brain injury

Answer 7

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

Question 8

Microglia

Answer 8

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

Question 9

Gitter cells

Answer 9

=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

Question 10

Spinal trauma

Answer 10

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.

Question 11

Inter-vertebral disc disease in chondrodystrophic breeds

Answer 11

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.

Question 12

Inter-vertebral disc disease in non-chondrodystrophic breeds

Answer 12

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

Question 13

Hansen’s type I vs. Hansen’s type II

Answer 13

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.

Question 14

Cervical stenotic myelopathy

Answer 14

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

Question 15

Cervical static stenosis

Answer 15

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

Question 16

Cervical vertical instability

Answer 16

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

Question 17

Wallerian Degeneration

Answer 17

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)

Question 18

Peripheral nerve damage and removal

Answer 18

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)

Question 19

CNS- axons don’t regenerate

Answer 19

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.

Question 20

Peripheral nerve regeneration

Answer 20

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.