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Created page with "* Neurons are particularly vulnerable to injury, due to their: ** High metabolic rate ** Small capacity to store energy ** Lack of regenerative ability ** Axons being very depend..."
* Neurons are particularly vulnerable to injury, due to their:
** High metabolic rate
** Small capacity to store energy
** Lack of regenerative ability
** Axons being very dependent on the cell body.
*** Axons cannot make their own protein as they have no Nissl substance.
*** The cell body produces the axon's protein and disposes of its waste.
*** Death or damage of the cell body causes axon degeneration.
* There are four ways in which neurons may react to insult:
*# Acute Necrosis
*# Chromatolysis
*# Wallerian Degeneration
*# Vacuolation
===Acute Necrosis===
* Acute necrosis is the most common neuronal response to injury.
* Causes of actue necrosis include:
** Ischaemia
*** Diminution of the blood supply causes a lack of nutrients and oxygen, inhibiting energy production. A decrease in the levels of ATP leads to:
***# Failure of the Na<sup>+</sup>/K<sup>+</sup>pumps, causing cell swelling and an increase in extracellular potassium.
***# Failure to generate NAD required for DNA repair.
** Hypoxia
** Hypoglycaemia
** Toxins, such as lead and mercury
====Laminar Cortical Necrosis====
* Laminar cortical necrosis refers to the selective destruction of neurons in the deeper layers of the cerebral cortex.
** These neurons are the most sensitive to hypoxia.
* The laminar cortical pattern of acute necrosis occurs in several instances:
*# Ischaemia
*#* For example, seizure-related ischaemia in dogs.
*# Polioencephalomalacia in ruminants
*#* Also called cerebrocortical necrosis or CCN.
*# Salt poisoning in swine
*# Lead poisoning in cattle
* It is most likely that gross changes will not be seen. When they are visible, changes may be apparent as:
** Oedema
*** Causes brain swelling, flattened gyri and herniation
** A thin, white, glistening line along the middle of the cortex.
*** In ruminants, this fluoresces with UV-light.
* Ultimately the cortex becomes necrotic and collapses.
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=F_KSsrch&kw=POLIOENCEPHALOMALACIA View images courtesy of Cornell Veterinary Medicine]
===Chromatolysis===
* Chromatolysis is the cell body’s reaction to axonal insult.
* The cell body swells and the Nissl substance (granular cytoplasmic reticulum and ribosomes found in nerve cell bodies) disperses.
** Dispersal of the Nissl substance allows the cell body to produce proteins for rebuilding the axon.
* IT IS NOT A FORM OF NECROSIS.
** It is an adaptive response to deal with the injury.
** It can, however lead to necrosis.
* Seen, for example, in grass sickness in [[Equine Alimentary System - Anatomy & Physiology|horses]] (equine dysautonomia).
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Display&imgID=13353 View images courtesy of Cornell Veterinary Medicine]
===Wallerian Degeneration===
* Wallerian degeneration is the axon’s reaction to insult.
* The axon and its myelin sheath degenerates distal to the point of injury.
* There are several causes of wallerian degeneration:
** Axonal transection
*** This is the "classic" cause
** Vascular causes
** Inflamatory reactions
** Toxic insult
** As a sequel to neuronal cell death.
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=F_KSsrch&kw=WALLERIAN View images courtesy of Cornell Veterinary Medicine]
====The Process of Wallerian Degeneration====
# '''Axonal Degeneration'''
#* Axonal injuries initially lead to acute axonal degeneration.
#** The proximal and distal ends separate within 30 minutes of injury.
#* Degeneration and swelling of the axolemma eventually leads to formation of bead-like particles.
#* After the membrane is degraded, the organelles and cytoskeleton disintegrate.
#** Larger axons require longer time for cytoskeleton degradation and thus take a longer time to degenerate.
# '''Myelin Clearance'''
#* Following axonal degeneration, myelin debris is cleared by phagocytosis.
#* Myelin clearance in the PNS is much faster and efficient that in the CNS. This is due to:
#** The actions of schwann cells in the PNS.
#** Differences in changes in the blood-brain barrier in each system.
#*** In the PNS, the permeability increases throughout the distal stump.
#*** Barrier disruption in CNS is limited to the site of injury.
# '''Regeneration''' [[Image:neuronalvacuolation1.jpg|thumb|right|150px|Neuronal vacuolation. Image courtesy of BioMed Archive]]
#* Regeneration is rapid in the PNS.
#** Schwann cells release growth factors to support regeneration.
#* CNS regeneration is much slower, and is almost absent in most species.
#** This is due to:
#*** Slow or absent phagocytosis
#*** Little or no axonal regeneration, because:
#**** Oligodendrocytes have little capacity for remyelination compared to Schwann cells.
#**** There is no basal lamina scaffold to support a new axonal sprout.
#**** The debris from central myelin inhibits axonal sprouting.
===Vacuolation===
[[Image:neuronalvacuolation2.jpg|thumb|right|150px|Neuronal vacuolation. Image courtesy of BioMed Archive]]
* Vacuolation is the hallmark of transmissible spongiform encephalopathies.
** For example, BSE and Scrapie.
* Vacuolation can also occur under other circumstances:
** Artefact of fixation
** Toxicoses
** It may sometimes be a normal feature.
[[Category:CNS Response to Injury]]
** High metabolic rate
** Small capacity to store energy
** Lack of regenerative ability
** Axons being very dependent on the cell body.
*** Axons cannot make their own protein as they have no Nissl substance.
*** The cell body produces the axon's protein and disposes of its waste.
*** Death or damage of the cell body causes axon degeneration.
* There are four ways in which neurons may react to insult:
*# Acute Necrosis
*# Chromatolysis
*# Wallerian Degeneration
*# Vacuolation
===Acute Necrosis===
* Acute necrosis is the most common neuronal response to injury.
* Causes of actue necrosis include:
** Ischaemia
*** Diminution of the blood supply causes a lack of nutrients and oxygen, inhibiting energy production. A decrease in the levels of ATP leads to:
***# Failure of the Na<sup>+</sup>/K<sup>+</sup>pumps, causing cell swelling and an increase in extracellular potassium.
***# Failure to generate NAD required for DNA repair.
** Hypoxia
** Hypoglycaemia
** Toxins, such as lead and mercury
====Laminar Cortical Necrosis====
* Laminar cortical necrosis refers to the selective destruction of neurons in the deeper layers of the cerebral cortex.
** These neurons are the most sensitive to hypoxia.
* The laminar cortical pattern of acute necrosis occurs in several instances:
*# Ischaemia
*#* For example, seizure-related ischaemia in dogs.
*# Polioencephalomalacia in ruminants
*#* Also called cerebrocortical necrosis or CCN.
*# Salt poisoning in swine
*# Lead poisoning in cattle
* It is most likely that gross changes will not be seen. When they are visible, changes may be apparent as:
** Oedema
*** Causes brain swelling, flattened gyri and herniation
** A thin, white, glistening line along the middle of the cortex.
*** In ruminants, this fluoresces with UV-light.
* Ultimately the cortex becomes necrotic and collapses.
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=F_KSsrch&kw=POLIOENCEPHALOMALACIA View images courtesy of Cornell Veterinary Medicine]
===Chromatolysis===
* Chromatolysis is the cell body’s reaction to axonal insult.
* The cell body swells and the Nissl substance (granular cytoplasmic reticulum and ribosomes found in nerve cell bodies) disperses.
** Dispersal of the Nissl substance allows the cell body to produce proteins for rebuilding the axon.
* IT IS NOT A FORM OF NECROSIS.
** It is an adaptive response to deal with the injury.
** It can, however lead to necrosis.
* Seen, for example, in grass sickness in [[Equine Alimentary System - Anatomy & Physiology|horses]] (equine dysautonomia).
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Display&imgID=13353 View images courtesy of Cornell Veterinary Medicine]
===Wallerian Degeneration===
* Wallerian degeneration is the axon’s reaction to insult.
* The axon and its myelin sheath degenerates distal to the point of injury.
* There are several causes of wallerian degeneration:
** Axonal transection
*** This is the "classic" cause
** Vascular causes
** Inflamatory reactions
** Toxic insult
** As a sequel to neuronal cell death.
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=F_KSsrch&kw=WALLERIAN View images courtesy of Cornell Veterinary Medicine]
====The Process of Wallerian Degeneration====
# '''Axonal Degeneration'''
#* Axonal injuries initially lead to acute axonal degeneration.
#** The proximal and distal ends separate within 30 minutes of injury.
#* Degeneration and swelling of the axolemma eventually leads to formation of bead-like particles.
#* After the membrane is degraded, the organelles and cytoskeleton disintegrate.
#** Larger axons require longer time for cytoskeleton degradation and thus take a longer time to degenerate.
# '''Myelin Clearance'''
#* Following axonal degeneration, myelin debris is cleared by phagocytosis.
#* Myelin clearance in the PNS is much faster and efficient that in the CNS. This is due to:
#** The actions of schwann cells in the PNS.
#** Differences in changes in the blood-brain barrier in each system.
#*** In the PNS, the permeability increases throughout the distal stump.
#*** Barrier disruption in CNS is limited to the site of injury.
# '''Regeneration''' [[Image:neuronalvacuolation1.jpg|thumb|right|150px|Neuronal vacuolation. Image courtesy of BioMed Archive]]
#* Regeneration is rapid in the PNS.
#** Schwann cells release growth factors to support regeneration.
#* CNS regeneration is much slower, and is almost absent in most species.
#** This is due to:
#*** Slow or absent phagocytosis
#*** Little or no axonal regeneration, because:
#**** Oligodendrocytes have little capacity for remyelination compared to Schwann cells.
#**** There is no basal lamina scaffold to support a new axonal sprout.
#**** The debris from central myelin inhibits axonal sprouting.
===Vacuolation===
[[Image:neuronalvacuolation2.jpg|thumb|right|150px|Neuronal vacuolation. Image courtesy of BioMed Archive]]
* Vacuolation is the hallmark of transmissible spongiform encephalopathies.
** For example, BSE and Scrapie.
* Vacuolation can also occur under other circumstances:
** Artefact of fixation
** Toxicoses
** It may sometimes be a normal feature.
[[Category:CNS Response to Injury]]