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