Flashcards in Tissue Injury and Repair 4 Deck (26):
Brain will move. Often see damage on opposite side as well as where brain was hit.
Axial, rotational and angular energy applied to the brain determine the severity of shear, tensile and compressive forces that cause neuronal and vascular injury.
Subarachnoid space- contains fluid
Pia mater- in contact with brain.
DURA MATER MUST BE REMOVED FROM BRAIN AND SPINAL CORD BEFORE FIXATION, OR IT WILL NOT WORK.
BLOOD BRAIN BARRIER
Comprised of capillary endothelial cells, basement membrane, astrocytic foot processes.
Formed structurally by tight junctions between endothelial cells.
Formed functionally by specialised transport systems in these cells- only certain molecules are transported.
In the cortex of the brain
Underneath the dura mater. Usually laceration of a vein- low pressure.
Haemorrhage beneath the arachnoid mater, in the subarachnoid space.
Outside the dura mater. Usually laceration of the meningeal artery- high pressure.
Degenerative changes to brainstem nuclei, becoming more severe if repeated.
More severe impact causes haematoma of subarachnoid space and/or parenchyma.
Could be caused by tumour.
Pooling of blood in venous sinuses of calvarium seen in response to trauma. Often seen as a post mortem change- there may be no actual damage to the skull or brain- check!
Torn by fractures or penetrating objects, including bone fragments, bullets.
As a general rule, acute nervous system injuries (such as laceration) are more disruptive than slowly developing injuries.
Provide structural support.
Form part of blood brain barrier.
Selective transfer of neurotransmitters.
Fluid and ionic homeostasis.
Uptake of excess neurotransmitters.
Undergo hypertrophy and hyperplasia in response to injury. GLIOSIS.
There are very few fibrocytes in the brain, so it cannot form scar tissue.
Astrocytes and few fibrocytes try to form fibrosis.
Little fibrosis is with penetrating trauma or around abscesses.
Astrocytes are the principal cells responsible for repair and scar formation in the brain- GLIOSIS (increase in glial cells)
With large defects, there may be a persistent cavity formed.
Fibrocytes ARE present in the meninges, so fibrous scar tissue can form if the meninges is affected.
Reactive astrocytes (seen in response to injury)
Long standing gliosis is more fibrillar.
'Macrophages of the brain'
make up <5% of glial cells.
Proliferate following injury, can transform in to brain macrophages.
Aggregates/clusters at small sites of injury are called microglial NODULES.
Macrophages which have ingested degenerate myelin (nerve sheath) and other debris eg. in liquefied necrotic area.
Can persist for months.
Can be extrinsic or intrinsic.
EXTRINSIC- Cars, kicks, crushing injury, penetrating objects.
Fracture most likely to be seen at thoracolumbar junction.
INTRINSIC- Disc prolapse, pathological vertebral fractures (eg. due to abscess, neoplasia).
Intervertebral disc disease most likely to be seen around thoracolumbar area as there is little extradural space, and the thoracic cord is protected by conjugal ligaments.
INTERVERTEBRAL DISC DISEASE
Seen in CHONDODYSTROPHIC dogs as young as 6 months.
Nucleus pulposus is replaced by cartilage, which increases pressure on annulus fibrosis.
Annulua fibrosis degenerates, protrusion can occur.
Sudden protrusion is likely.
HANSEN TYPE I HERNIATION
Seen in chondodystrophic animals. Degenerative changes to the vertebral discs can be seen in animals as young as 6 months.
Cartilagenous nucleus pulposus is released from the annulus fibrosis and enters the spinal canal, where it compresses the spinal cord.
HANSEN TYPE II HERNIATION
Seen in NON-CHONDODYSTROPHIC animals.
Age related metaplasia of nucleus pulposus means it gradually loses it's elasticity.
This causes increased stress on the annulus fibrosis, which protrudes up in to the spinal canal, compressing the spinal cord.
Seen clinically by 8-10 years of age.
CERVICAL STENOTIC MYELOPATHY
Myelo- spinal cord.
Seen in horses due to malformation or malarticulation of cervical vertebrae.
Seen in young, rapidly growing breeds (dogs also- large breed, male, rapid growing. See both forms).
Neck can be submitted to pathologist for PM removal of spinal cord- should NOT be done in practice.
Two types are seen:
1. Cervical static stenosis.
2. Cervical vertebral instability.
CERVICAL STATIC STENOSIS
Narrowing of spinal canal due to bone formation.
Usually in horses aged 1-4 years.
CERVICAL VERTEBRAL INSTABILITY
DYNAMIC- narrowing of the spinal canal is only seen when neck is flexed.
Usually in horses aged 8-18 months of age.
Result of trauma, classically seen in compression.
Follows myelinated axonal disruption in the brain, spinal cord or nerves.
SEQUENCE OF DEGENERATION AND REMOVAL OF SEVERED AXONS.
First described in peripheral nerves.
Everything distal to the trauma degenerates and myelin is removed by phagocytosis- 'digestion chambers'.
Histologically- Digestion chambers containing myelin etc.
Axonal spheroid- swollen axon. Not always seen, but are a useful indicator.
After Wallerian degeneration, CNS axons do NOT regenerate.
Oligodendrocytes prevent axonal budding by providing myelin proteins (sheath) for up to 50 axons each.
No endoneurium (no fibrocytes).