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===Ischaemic Damage===
* The CNS is particularly sensitive to ischaemia, because it has few energy reserves.
* The CNS is protected by its bony covering.
** Despite offering protection, the covering also makes the CNS vulnerable to certain types of damage, for example:
*** Damage due to fractures and dislocation.
*** Damage due to raised intracranial pressure.
**** Raised intracranial stimulates a compensatory increase in blood flow, further raising intracranial pressure. This stimulates a further increase in blood flow, and the cycle continues until intracranial pressure is so high that blood flow is impeded.
***** The result of this is '''ischaemia'''.
* Survival of any cell is dependent on having sufficient energy.
** Ischaemia causes cell death by impeding energy supply to cells.
*** Cells directly affected by ischamia die rapidly.
**** For example, those suffering a failure of pefusion due to an infarct.
*** Neurons surrounding this area of complete and rapid cell death exist under sub-optimal conditions and die over a more prolonged period.
**** This area of gradual death is known as the '''lesion penumbra'''.
**** There are several mechanisms implicated in cell death in the penumbra:
****# Increase in intracellular calcium
****# Failure to control free radicals
****# Generation of nitrogen species (e.g NO and ONOO) are the main damaging events.
===Oedema===
* There are three types of cerebral oedema:
*# '''Vasogenic oedema'''
*#* Vasogenic oedema follows vascular injury.
*#* Oedema fluid gathers outside of the cell.
*#* This is the most common variation of cerebral oedema.
*# '''Cytotoxic oedema'''
*#* Cytotoxic oedema is due to an energy deficit.
*#** The neuron can’t pump out sodium and water leading to swelling within the cell.
*# '''Interstitial oedema'''
*#* Associated with hydrocephalus.
*#* This type of cerebral oedema is of lesser importance.
* One serious consequence of oedema is that the increase in size leads to the brain trying to escape the skull.
** This causes herniation of the brain tissue.
** The most common site of herniation is at the foramen magnum.
*** The medulla is compressed at the site of the respiratory centres, leading to death.
===Demyelination===
* Demyelination is the loss of initially normal myelin from the axon.
* Demyelination may be primary or secondary.
====Primary Demyelination====
* Normally formed myelin is selectively destroyed; however, the axon remains intact.
* Causes of primary demyelination:
** Toxins, such as hexachlorophene or triethyl tin.
** Oedema
** Immune-mediated demyelination
** Infectious diseases, for example canine distemper or caprine arthritis/encephalitis.
====Secondary Demyelination====
* Myelin is lost following damage to the axon.
** I.e. in [[CNS Response to Injury - Pathology#Wallerian Degeneration|wallerian degeneration]]
===Vascular Diseases===
* Vascular diseases can lead to complete or partial blockage of blood flow which leads to ischaemia.
** Consequences of ischaemia depend on:
**# Duration and degree of ischaemia
**# Size and type of vessel involved
**# Susceptibility of the tissue to hypoxia
* Potential outcomes of vascular blockage include:
** Infarct, and
** Necrosis of tissue following obstruction of its blood supply.
* Causes include:
** Thrombosis
*** Uncommon in animals but may be seen with DIC or sepsis.
** Embolism. e.g.
*** Bone marrow emboli following trauma or fractures in dogs
*** Fibrocartilaginous embolic myelopathy
** Vasculitis, e.g.
*** Hog cholera (pestivirus)
*** Malignant catarrhal fever (herpesvirus)
*** Oedema disease (angiopathy caused by E.coli toxin)
===Malacia===
* Malacia may be used:
** As a gross term, meaning "softening"
** As a microscopic term, meaning "necrosis"
* Malacia occurs in:
** Infarcted tissue
** Vascular injury, for example vasculitis.
** Reduced blood flow or hypoxia, e.g.
*** Carbon monoxide poisoning, which alters hemoglobin function
*** Cyanide poisoning, which inhibits tissue respiration
[[Category:CNS Response to Injury]]