Download Neuronal necrosis

Gitter cells
• Microglia function as phagocytes and likely part of the
monocyte phagocytic system. They are chiefly perivascular in
white matter and perivascular and perineuronal in gray matter.
• If inactive, the microglia contain small, round or rod-shaped
hyperchromatic nuclei. If active and phagocytic, the cytoplasm
becomes foamy due to phagocytosis if lipid and water. These
larger foamy or vacuolated cells are termed " gitter cells" or "
compound granule cells ". Proliferation of microglia in some
viral diseases results in small nodules called glial nodule.
These cells, not oligodendroglia, may indulge in
neuronophagia of degenerate neurons.
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Gitter cells
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Gitter cell, Myelin basic
protein IHC
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Neuronophagia
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Microglial nodule
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Ependymal cells and undifferentiated glial
cells- prominent in newborn animals
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Ependymal cells
• Ependymal cells line the
ventricles, choroid plexuses
and central canal.
Production and flow of CSF
are modified by ependymal
cells.
• Inflammation (ventriculitis
or choroid plexitis) or
neoplasia can result in CSF
disturbances of pressure
and/or volume.
• Granular ependymitis
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Extragranular layer10
Perivascular lymphocytic cuffing
• There is a space between the CNS
parenchyma and stroma and the blood
vessels with limited supporting framework.
• This is the perivascular space causing
perivascular lymphocytic infiltrations or "
cuffing".
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• Virchow-Robin
space
(Perivascular
space)
• Neuroectoder
mal and
mesodermal
derivation
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Perivascular lymphocytic cuffing
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Perivascular eosinophilic cuffing
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Neuronal necrosis
• Neurons are very susceptible to inadequate
nutrients and oxygen and degeneration and
necrosis result.
• The order of sensitivity to lack of oxygen is :
neurons, oligodendroglia, astrocytes, and
microglia.
• Some neurons are more susceptible to
hypoxia than others, e.g. neocortical neurons
have a 5 minute survival, basal nuclei- 10
minutes.
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Necrosis of neuron groups
• Focal or laminar
• Focal necrosis may result from vascular compromise
(infarction). Neurons and glia are both involved
usually.
• Focal necrosis of specific nuclei may occur with some
toxicities, e.g. pallidonigral necrosis with yellow star
thistle poisoning of horses.
• Causes of neuron necrosis include: cardiac arrest,
cerebral embolism and thrombosis and ruptured
aneurysm which lead to infarction, and toxins (lead,
mercury, plant toxins).
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Laminar cortical necrosis
• Occurs due to the extreme susceptibility of the
second and third layers of the cerebral cortex to
hypoxia.
• Causes of laminar cortical necrosis include:
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–
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Carbon monoxide poisoning
Hypoglycemia
Salt poisoning in swine
Thiamine deficiency in cattle and sheep
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Laminar cortical necrosis, Polioencephalomalacia
(PEM), B1 deficiency in cattle
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Laminar cortical necrosis, salt
poisoning in pigs
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Malacia
• If larger areas undergo necrosis, the gross change is
termed malacia. This is liquefactive necrosis.
• The sequence of events is as follows:
– 2-5 days: grossly softened and discolored yellow
– Liquefaction in 7-14 days
– If the area of necrosis is large, there is a cavity lined by glia;
if small, the space may be obliterated by gliosis
– Large numbers of macrophages or gitter cells may be
present
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Peripheral nerve damage and repair
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Wallerian degeneration
• When a nerve fiber is severed or damaged, the
breakdown of the axon and its myelin sheath is
termed Wallerian degeneration. The process is
termed degeneration although the axon and myelin
are really destroyed or die.
• Causes of Wallerian degeneration:
– Compression and crushing by trauma, abscesses or
neoplasms
– Transection
– Stretching
– Intoxication (lead, mercury, arsenic)
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Multiple digestion chambers (arrows)
containing axonal fragments and
macrophages
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Function of myelin sheath
• Increase the velocity of impulse conduction.
• Protect the portion of the nerve cell it
surrounds.
• Relate the nutrition of the nerve cell.
• Necessary for repair and regeneration.
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Demyelination
• Disorders of oligodendroglia or schwann cells can produce
myelin sheath defects. Although the axon is initially intact, it is
eventually altered and destroyed secondary to myelin defects.
Whether demyelination or axonal degeneration occurs first in
some diseases is not clear and there is some overlap.
• There are two categories of myelin disease:
– Demyelinating (myelinoclastic)
– Dysmyelinogenesis disorders of myelin formation such as
leukodystrophies
• Demyelination stimulates glial proliferation.
• Demyelinated nerves may regenerate but most demyelinating
diseases are progressive.
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Demyelination of cerebellum, canine distemper
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Demyelination, LFB-CEV
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GFAP
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Axonal degeneration
• Axonal degeneration affects the entire neuron but
degeneration usually begins at the distal end of the
neuron and proceeds toward the cell body. This is
called "dying back".
• Schwann cell proliferation in the area of axonal
degeneration occurs but less than in Wallerian
degeneration. Regeneration and recovery are
possible if the degeneration process is stopped in
time.
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Alterations of Neurons, glial
cells and other components
in the nervous system
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Neurons
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Central chromatolysis VS
peripheral chromatolysis
Neuronophagia
Acute necrosis
Laminar cortical necrosis
Intranuclear or
cytoplasmic inclusion
body
Vacuolar change： BSE,
Scrapie
• Abnormal accumulations:
lipofuscin, storage disease
• Deposition of extraneous
pigment: hematin pigment,
ferrugination or iron
incrustation
• Axonal degeneration
• Hytrophic changes: Bi- or
multinucleated neuron
• Wallerian degeneration
(axonal alteration)
• Axonal balls
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Astrocytes
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Hypertrophic astrocytes (Gemistocytes)
Rothensal fibers
Gliosis (astrocytic gliosis)
Viral inclusion: CD
Corpora amylacea
Chronic degenerative change: lipofuscin
Abnormal accumulations:
mucopolysaccharidiosis
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Oligodendrocytes
•
•
•
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Satellitosis
Viral inclusions: papovavirus
Acute swelling (hydropic change) of the
cytoplasm-- autolytic change
Convert to astrocytes and participate in glial
scar formation
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Microglia
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“Gitter” (=lattice in German) cells and
“Compound granular corpuscles” (French)
Microglial nodule
Neuronophagia
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Ependymal cells
• Granular ependymitis
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Other alterations
• Malacia
• Infarct
• Perivascular lymphocytic
cuffing
• Demyelination
• Vascular endotheliumhypertrophy (HC), viral
inclusions (ICH, canine
parvoviral infection)
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Hemorrhage
Edema
Abscess- bacterial infection
Granuloma- mycotic
infection
• Primary tumors or
metastasizing tumors
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In coming issue…..
Comparative Pathology and Emerging
Zoonosis
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